Scholars All Years - Rita Allen Foundation

2025

Alexander Chamessian +
Washington University School of Medicine in St. Louis

Alexander Chamessian

Assistant Professor, Anesthesiology

B.Sc., Stony Brook University

M.D., Ph.D., Duke University School of Medicine

Chronic pain affects more than 50 million Americans, and current treatments often rely on opioids, which can be addictive and ineffective for many people. The Chamessian Lab is exploring a promising new way to relieve pain using an emerging therapeutic modality called targeted protein degradation (TPD), which eliminates protein targets rather than just blocking them. This project will apply TPD to the voltage-gated sodium channels NaV1.7 and NaV1.8, both of which are key mediators of pain in humans. The proposed work builds on foundational in vitro results from the Chamessian Lab showing for the first time that NaV1.7/8 are amenable to TPD using small molecule effectors called PROTACs. Now, Alexander Chamessian and his team will 1) test the ability of PROTAC-mediated TPD of NaV1.7/8 to produce analgesia in vivo using preclinical animal models, and 2) develop new tools to more selectively direct TPD to pain-generating neurons (nociceptors). Taken together, this work is poised to deliver novel, non-addictive degrader analgesics to bring much needed relief to the millions of people suffering from chronic pain.
Lamia Wahba +
The Rockefeller University

Lamia Wahba

Assistant Professor, Genetics and Genomics

B.Sc., College of William and Mary

Ph.D., Johns Hopkins University

In the last months of 1944, towns in Western Netherlands plunged into the Hongerwinter, a six-month period of acute famine brought on by World War II. Nearly six decades later, a landmark study revealed that descendants of the Dutch survivors suffered adverse health effects two generations down. How did hunger impact their grandchildren’s lifespan?

External factors such as diet and stress have been linked to adverse consequences transmissible to offspring. This notion that environmentally-induced changes in an organism’s physiology can be passed on to offspring—once dismissed as heresy—has now gained widespread acceptance. However, critical questions on the prevalence and stability of such induced traits remain. Whether mechanisms driving these seemingly non-genetic changes could enable more rapid evolution in response to new environments than genetic alterations alone remains unclear. Addressing these questions drives research in the Wahba Lab, where Lamia Wahba and her team seek to answer a fundamental question facing biologists today: Do we need to radically rethink our views on inheritance to account for nongenetic mechanisms?
Deepshika Ramanan +
Salk Institute for Biological Studies

Deepshika Ramanan

Assistant Professor, Molecular Biology

B.Sc., Winona State University

Ph.D., New York University

Maternal protection of offspring through milk is fundamental across mammals, yet the underlying immune mechanisms remain poorly understood. Breastmilk contains immune factors such as antibodies that not only defend against pathogens but also shape the infant’s gut immunity and influence lifelong health. However, what determines the immune composition of breastmilk and how it impacts infant intestinal immunity is still unclear. The Ramanan Lab studies the entero-mammary axis—the bidirectional communication between the gut and mammary gland—to understand how maternal immunity is transferred through milk. Using multi-omic approaches, the lab aims to uncover how immune cells and other signals from the gut influence maternal mammary gland and milk composition, and how these components protect the offspring from infections and autoimmune diseases.
Christopher Lapointe +
Fred Hutchinson Cancer Center

Christopher Lapointe

Assistant Professor, Basic Sciences Division

B.A., Colby College

Ph.D., University of Wisconsin-Madison

Cells contain tens of millions of protein molecules responsible for conducting the many functions required for life, including sending nerve signals, tightening muscles, fighting off viruses and more. These proteins are made by tiny molecular machines called ribosomes, which use the information stored in genes to build the proteins found in cells. At any given moment, millions of ribosomes must find the correct set of genetic instructions and start reading them at exactly the right spot. When this critical process goes awry, it can lead to many diseases, including cancer, developmental disorders, autoimmune diseases, and neurodegenerative conditions.

The Lapointe Lab uses cutting-edge technologies that capture ‘molecular movies’ of individual ribosomes at work, to see and understand how healthy cells control protein production and how this control breaks down in disease. These discoveries will help reveal potential new strategies for treating disorders connected to ribosomal dysfunction.
Martin Taylor +
Brown University

Martin Taylor

Assistant Professor, Pathology and Laboratory Medicine

Milton E. Cassel Scholar

B.S.E., Princeton University

M.D., Ph.D., Johns Hopkins University School of Medicine

Genes make up only 2 percent of the human genome. In contrast, half the genome is around two million copies of the same few transposon sequences, which for years were relegated as “junk DNA.” Transposons are virus-like, self-copying DNA parasites. In humans, there is one class of active transposon, called LINE-1. Among hundreds of thousands of inactive copies and fragments, humans inherit 150–200 active copies of LINE-1, which are repressed in healthy tissues by multiple redundant mechanisms. In cancer, autoimmunity, and diseases of aging such as Alzheimer’s, LINE-1 escapes repression and contributes to disease pathology by mutating the genome and causing inflammation. The goals of the Taylor Lab are to 1) understand how LINE-1 works in detail and how much of a contribution it makes in these diseases, 2) develop new strategies to target LINE-1 for prevention and therapy, and 3) develop new diagnostics to find disease earlier, where interventions are most effective.
Allan-Hermann Pool +
UT Southwestern Medical Center

Allan-Hermann Pool

Assistant Professor, Neuroscience, Anesthesiology and Pain Management

B.Sc., Tallinn University of Technology

Ph.D., University of California, Berkeley

Animals have evolved the ability to discriminate between different types of tissue injuries and perceive them as distinct pain states. The Pool Lab seeks to understand cellular mechanisms through which the spinal cord translates tissue damage into central pain perception and orchestrates adaptive and maladaptive pain behaviors. To this end, the Pool Lab is studying the functional role of diverse spinal cord output neuron classes that link the spinal cord to the central brain and give rise to all pain perception below the neck. Furthermore, the lab aims to develop a new therapeutic avenue to selectively mute pain-conveying spinal cell types based on cellular features that differentiate them from the rest of the delicate spinal cord circuitry. Consequently, Allan-Hermann Pool and his team hope to identify new cellular and molecular targets for precision control of the perception of pain.
Alex Johnson +
Brandeis University

Alex Johnson

Assistant Professor, Biochemistry

B.A., Reed College

Ph.D., Stanford University

All cellular life is defined by membranes. At the edge of the cell, the plasma membrane forms a barrier against external insults, and internally, organellar membranes compartmentalize crucial cellular processes. Proteins embedded within membranes allow for the regulated passage of biomolecules and communication within and between cells. As a result, membranes are a focal point of immune signaling pathways and a chief target of pathogens that seek to destroy cells. Alex Johnson discovered that an immune signaling mechanism used by human cells is billions of years older than expected and deployed by bacteria to defend against their major pathogens, bacteriophages. In cells, this mechanism relies on an incredible class of proteins that form gigantic pores in membranes, effectively “poking holes” that induce cell death and the secretion of immune signaling molecules. By studying bacterial homologs of these pore-forming proteins, Johnson’s work established a new frame of reference to understand how these proteins work and yielded unforeseen insights into their mechanism of regulation in human cells. The broad goal of his lab’s research program is to answer stubborn problems of immunology using a comparative evolutionary analysis. Currently, the lab of Microbes and Biochemistry at Brandeis University is focused on applying a pan-species analysis to reveal the full breadth of mechanisms used by pore-forming proteins and applying this knowledge to develop pore-forming proteins as a new therapeutic modality.

2024

Alexander Meeske +
University of Washington

Alexander Meeske

Assistant Professor, Microbiology

B.Sc., University of Connecticut

Ph.D., Harvard University

All organisms have evolved strategies to cope with the threat of invasion by parasites. Bacteriophages—viruses that infect and kill bacteria—impose strong pressures on their hosts, giving rise to diverse anti-viral defenses, including restriction-modification and CRISPR-Cas systems. The well-documented utility of these systems for genetic engineering, combined with the rise of facile microbial genome sequencing, has ushered in a renaissance in the study of prokaryotic immune systems. The Meeske Lab has developed native host models to investigate the interfaces between diverse immune effectors, prokaryotic hosts, and the viruses that infect them. Using these tools, we will expand our understanding of the ways in which bacterial immune systems are controlled by their hosts, the cues to which they naturally respond, and the counter-defense strategies taken by bacteriophages to overcome them. We anticipate that these efforts will refine the toolkit of modern molecular biology and inform bacteriophage-based strategies for antimicrobial intervention.
Longzhi Tan +
Stanford University

Longzhi Tan

Assistant Professor, Neurobiology

B.Sc., Massachusetts Institute of Technology

Ph.D., Harvard University

How do cells in our body develop highly specialized functions, and how do they degenerate as we age? Genome architecture—the 3D folding of 2 meters of DNA into a 10-μm nucleus to control gene expression—plays a critical role in both normal physiology and many diseases. To measure this structure, we built an optics-free “microscope” that uses DNA sequencing to measure pairwise distances between molecules, solving the first 3D structure of the human genome and discovering highly specialized genome architecture across the body (brain, nose, eye, blood, etc.) and across the life span. Most notably, we demonstrated 3D genome “structure typing” —just by looking at a cell’s DNA structure, one can tell what type of cell it is. We also found that these intricate structures drive neurodevelopment and change progressively over around 100 years. The Tan Lab’s work, therefore, reveals a new physical dimension of development and aging.
Kara Marshall +
Baylor College of Medicine

Kara Marshall

Assistant Professor, Neuroscience

B.Sc., Texas A&M University

Ph.D., Columbia University

Internal organs move, stretch, and squeeze as part of their normal functions. The mechanical forces caused by these movements are detected by the nervous system to generate important sensations, such as a full bladder, and to govern physiological processes themselves, like urination. Unfortunately, during disease, internal forces can also cause pain. The Marshall Lab seeks to understand the molecules and cell types that mediate the detection of mechanical force within the body, in both healthy and disease states. We hope to uncover fundamental mechanisms of internal mechanosensation, and potentially pave the way for new therapies targeting internal pain.
Katelyn Sadler +
University of Texas at Dallas

Katelyn Sadler

Assistant Professor, Neuroscience

B.Sc., University of Pittsburgh

Ph.D., Duquesne University

Trillions of bacteria live in and on the surface of the human body. These microorganisms and the metabolites they produce are collectively termed the microbiome and are known to interact with various host cells. We are just beginning to deconstruct the complex, bi-directional signaling that occurs between microbiomes and the peripheral nervous system, but we believe that this type of work will provide fundamental insight into sensory processes that occur in health and disease. In particular, the Sadler Lab is very interested in understanding how tissue-specific microbiomes contribute to normal sensation and how changes in the microbiome contribute to chronic pain. Using a combination of preclinical animal models, healthy human tissues, and patient samples, we ultimately aim to identify novel microbiome-related therapeutic targets for pain management.
Daniele Canzio +
University of California, San Francisco

Daniele Canzio

Milton E. Cassel Scholar

Assistant Professor, Neurology

B.Sc., University of California, Santa Barbara

Ph.D, University of California, San Francisco

The establishment of functional neural circuits relies on the ability of neurons to discriminate self from non-self. This self/non-self discrimination requires the generation of an astonishing number of cell-surface protein “barcodes” that uniquely “mark” individual neurons with their own identity. Neurons expressing the same barcodes repel one another, while neurons expressing different barcodes are allowed to interact. Given that a human brain houses billions of neurons, how this remarkable number of cell-surface barcodes is generated from a single genome remains a mystery. Research at the Canzio Lab points to a new role of genome architecture and its dynamics in the regulation of the transcriptional diversity underlying the barcoding strategy of neurons to recognize self from non-self, providing a novel mechanism to achieve cellular individuality. Our findings have broad implications, from uncovering the molecular basis of neural wiring during brain development to revealing new insights on the role of genome structure in defining cellular fate and function.
Erica Pratt +
Boston University

Erica Pratt

Assistant Professor, Biomedical Engineering

B.Sc., Carnegie Mellon University

Ph.D., Cornell University

The peripheral circulation and other biofluids contain a variety of tumor-derived analytes, ranging from intact cells and exosomes to free nucleic acids. These ‘liquid biopsies’ offer a readily accessible and minimally invasive strategy for taking real-time snapshots of a dynamic tumor landscape. Critically, liquid biopsies can improve patient outcomes by revealing therapeutically actionable subpopulations missed using conventional tissue biopsies. However, these circulating biomarkers are extremely rare and require sophisticated strategies to isolate and characterize them. The Pratt Laboratory develops enabling technologies for ultra-sensitive multiplexed profiling of liquid biopsies for cancer monitoring and precision medicine. Our work leverages next-generation genetic tools in combination with techniques from bioengineering and chemical biology.
Elizabeth Pollina +
Washington University School of Medicine in St. Louis

Elizabeth Pollina

Assistant Professor, Developmental Biology

B.A., Princeton University

Ph.D., Stanford University

A striking feature of the nervous system is its continual adaptation to environmental cues throughout the lifespan of an animal. Environmental stimuli trigger changes in neuronal activity that, in turn, induce transcriptional programs controlling adaptive modifications to neuronal circuitry. Stimulus-induced transcription is, however, a risky endeavor. During transcription, DNA is cut, unwound, and reannealed in a process that has the potential to create mutations. Across a lifetime, a neuron may undergo this process millions of times. How do animals balance the benefits of inducible transcription for plasticity with the intrinsic risks it poses to their genetic code? Our knowledge of genome integrity derives primarily from dividing cells grown in culture conditions. We lack a fundamental understanding of how neurons repair genomic insults in vivo and how the dynamic stimuli neurons receive further impinge on the genome. The Pollina Lab leverages tools and techniques from neuroscience, epigenetics, and DNA repair to advance our knowledge of genome fidelity in the nervous system. We characterize the pathways downstream of external signaling cues that preserve neuronal genomes in short- versus long-lived species. We examine how lifestyle factors, such as diet and sleep, impact signal-dependent transcription and genome repair across time. Ultimately, we aim to use this knowledge to design strategies that prevent or even correct molecular damage in aged and diseased neurons.

2023

Hongying (Hoy) Shen +
Yale University

Hongying (Hoy) Shen

Assistant Professor, Cellular and Molecular Physiology

B.S., Nanjing University

Ph.D., Yale University

The nervous system harbors numerous metabolic enzymes and transporters that play important roles in brain physiology. However, the functions of hundreds of these, including those genetically linked to neurological and psychiatric disorders, remain poorly understood. To bridge this knowledge gap and overcome technical barriers, the Shen lab has devised a suite of mass spectrometry metabolomics-based biochemistry methods, combining in vitro activity-based metabolomics with neuronal cellular metabolomics screening, to simultaneously investigate multiple disease-associated genes in a multiplexed format. This “deorphanization” pipeline holds the promise of uncovering novel brain biochemistry governed by these orphan metabolic genes, elucidating their impact on neuronal metabolism and synaptic transmission. Focusing on disease-associated genes might yield insights into the pathologies of brain disorders and facilitate the development of new diagnostics and therapeutics.
William Renthal +
Brigham and Women's Hospital, Harvard Medical School

William Renthal

Associate Professor, Neurology; and Director, Headache Research

Ph.D., University of Texas Southwestern Medical Center

M.D., University of Texas Southwestern Medical Center

In conjunction with Margaret and William R. Hearst III

The Renthal lab studies the genomic and epigenomic mechanisms that contribute to conditions related to refractory headache and facial pain. This work aims to reveal molecular features that are unique to pain-related cells and circuits that could be used to develop novel strategies for pain therapeutics with fewer side effects. Dr. Renthal also co-directs the Harvard PRECISION Pain Center, an NIH-funded network of pain clinicians and scientists who are leveraging advanced multi-omic technologies to characterize the specific cell types and states associated with pain using human samples. Together, this work aims to improve translation of basic research discoveries into safer treatments for patients with refractory headache and/or pain conditions.
Nicole M. Martinez +
Stanford University

Nicole M. Martinez

Assistant Professor, Chemical and Systems Biology; Developmental Biology

B.S., University of Puerto Rico-Mayaguez

Ph.D., University of Pennsylvania

Messenger RNAs (mRNAs), the instructions to make proteins, are composed from a 4-letter alphabet of RNA bases. These bases are extensively chemically modified to create new letters in the alphabet that change the meaning of the message. These changes can impact the fate and function of mRNAs in cells. The full collection of RNA modifications in cellular mRNAs represents a previously unappreciated layer of gene regulation on top of what is hard-wired in our genome. The Martinez lab studies how these chemical modifications are added very early when mRNAs are “born,” and how they impact how mRNAs are processed and interpreted in cells. RNA modifications have an important role in health and disease: many RNA modifying enzymes have been associated with a wide range of human diseases, particularly neurodevelopmental disorders, and cancer. Our goal is to connect molecular functions of RNA modifications to normal and disease traits using innovative high-throughput sequencing methods, RNA biochemistry, and model systems.
Emerson Krock +
McGill University

Emerson Krock

Assistant Professor, Dental Medicine and Oral Health Sciences

B.Sc., McGill University

Ph.D., McGill University

Fibromyalgia is a chronic, whole-body pain disorder. Despite having a clinical diagnosis for decades, the underlying causes remain poorly understood. During a postdoctoral fellowship, Dr. Krock and colleagues found that IgG antibodies from fibromyalgia patients cause mice to develop signs of pain, but antibodies from pain-free people do not. The fibromyalgia antibodies bind to satellite glia cells, which surround pain-sensing neurons, and the levels of these antibodies are higher in fibromyalgia patients with more pain. These results suggest a subset of fibromyalgia pain could be mediated by autoantibodies—that is, antibodies attacking parts of our own body. However, why these autoantibodies develop remains unclear. The Krock lab at McGill University is investigating how fibromyalgia autoantibodies develop. One possibility is that altered gut bacteria stimulate an antibody-generating immune response, and if these antibodies recognize molecules similar enough to molecules found on satellite glia, then an autoantibody response could occur.
Lucas Farnung +
Harvard Medical School

Lucas Farnung

Milton E. Cassel Scholar

Assistant Professor, Cell Biology

B.Sc., University College London

Dr. rer. nat., Ludwig Maximilian University of Munich

Lucas Farnung has been designated the Milton E. Cassel Scholar for the 2023 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

Each human cell takes on an extraordinary feat, as it compacts its two-meter-long genome into a nucleus that is merely a few microns in size. Yet, our genetic material must remain accessible, ready to be read by the cell’s molecular machinery. To mitigate this conflict, the genomic DNA is spooled like yarn around specialized proteins called histones. Together, histones and the DNA form a structure called chromatin, akin to delicate beads on a string. The Farnung lab studies how a cellular machine called RNA polymerase II navigates through chromatin and generates blueprints of the DNA in a process called transcription. We use a combination of biophysical methods, machine learning, and structural biology approaches. Elucidating transcription through chromatin is important to understand how cells develop, morph into diverse types—like heart or liver cells—and react to the environment. With many cancers linked to dysregulated chromatin transcription, a deeper grasp of this process is vital for novel cancer therapy development.
Jesse Dixon +
Salk Institute for Biological Studies

Jesse Dixon

Assistant Professor, Gene Expression Laboratory

A.B., Princeton University

Ph.D., University of California San Diego

M.D., University of California San Diego

The Dixon lab is interested in how the spatial organization of genomes affects the acquisition and impact of mutations in cancer. Our genomes are 3 billion base pairs in length and must be compacted into the nucleus of every cell in our body. How our genomes are organized in cells has a major impact on diverse processes, from the expression of genes to the replication of DNA as cells divide. In cancer, our genomes are bombarded with mutations, some of which break and shuffle the genomes creating a mosaic of how these genomes appear in healthy cells. When our genomes are shuffled in cancer cells, this often can place cancer-causing genes in novel environments with altered spatial organization, which can lead to aberrant gene activation that drives the growth of cancer cells. We are interested in understanding where and when such altered gene regulation events occur and understanding what critical factors facilitate altered gene activation in cancer genomes.
Neil Dani +
Vanderbilt University

Neil Dani

Assistant Professor, Cell and Developmental Biology

B.S., University of Rochester

M.S., New York Medical College

Ph.D., Vanderbilt University

The Dani lab researches the choroid plexus, a fascinating and understudied structure in the brain that generates cerebrospinal fluid and nourishing substances that support brain health throughout life. Recently with collaborators, we generated detailed maps of the choroid plexus, which reveal the cellular sources of the nourishing substances and several additional cell types, suggesting previously unappreciated functions. We believe that the breakdown of these cellular functions contributes to neurological and neurogenerative disorders such as Alzheimer’s disease, and that further research could provide novel insights into potential new prevention methods or treatments. To investigate, we are using cutting edge imaging tools that enable us to directly visualize the activity of choroid plexus cells in real time.
Seungwon (Sebastian) Choi +
University of Texas Southwestern Medical Center

Seungwon (Sebastian) Choi

Assistant Professor; Psychiatry, Neuroscience, Anesthesiology, and Pain Management

B.S., Korea Advanced Institute of Science and Technology

M.S., Korea Advanced Institute of Science and Technology

Ph.D., Harvard University

In conjunction with Margaret and William R. Hearst III

Each day we experience myriad somatosensory stimuli—hugs from loved ones, warm showers, a mosquito bite, and sore muscles after a workout. These tactile, thermal, itch, and nociceptive signals are detected by sensory neurons innervating the skin, propagated into the spinal cord, and transmitted to the brain via ascending somatosensory pathways. Primary sensory neurons that innervate the skin and detect a wide range of somatosensory stimuli have been identified and well-characterized. In contrast, very little is known about how peripheral signals are integrated and processed within the spinal cord and how these signals are conveyed to the brain to generate somatosensory perception and behavioral responses. The Choi lab aims to determine the developmental logic, functional organization, and dysfunction of ascending somatosensory circuitry. Our lab explores these exciting areas using new mouse genetic tools in conjunction with advanced molecular, anatomical, physiological, and behavioral approaches.
Victoria Abraira +
Rutgers, The State University of New Jersey

Victoria Abraira

Assistant Professor, Cell Biology and Neuroscience

B.S., University of Southern California

Ph.D., Harvard University

The Abraira lab proposes a basic blueprint for how spinal cord circuits instantiate top-down emotional context into the modulation of somatosensory input before it even reaches the brain. This work impacts our fundamental understanding of the emotional and attentional aspects of somatosensation and contributes to the emerging picture of the sophistication of contextual processing in the spinal cord and peripheral sensory organs. This work supports the idea of spinal cord and associated peripheral circuits as therapeutic targets for treating conditions affecting somatosensory dysfunctions, like acute and chronic pain. While this specific research project focuses on one neuromodulatory signal, oxytocin, the same blueprint is currently being applied to other modulatory networks implicated in pain modulation, including serotonin, dopamine, norepinephrine, and endocannabinoids.

2022

Maria Antonietta Tosches +
Columbia University

Maria Antonietta Tosches

Assistant Professor; Department of Biological Sciences

Ph.D., European Molecular Biology Laboratory, Germany

M.S., University of Pisa and Scuola Normale Superiore, Italy

The stunning complexity of our brain is the result of a long journey, that started when squishy and brainless aggregates of cells—the first animals—appeared on Earth over 700 million years ago. Understanding how our brain evolved can shed light on fundamental principles underlying its organization and function. The Tosches lab investigates the evolution of the cerebral cortex, the part of our brain associated with advanced cognition. Focusing on neuron types as units of evolutionary change, we discovered that the mammalian cerebral cortex has a unique neuronal repertoire without clear counterparts in other vertebrates. Our future goal is to understand how changes of developmental programs and gene regulation contributed to the emergence of these new types of neurons in mammals.
Ryan A. Flynn +
Boston Children’s Hospital and Harvard University

Ryan A. Flynn

Assistant Professor; Pediatrics and the Stem Cell and Regenerative Biology Department

M.D., Ph.D., Stanford University, School of Medicine

B.S., Massachusetts Institute of Technology

Life is made up of many different types of biopolymers such as DNA, RNA, proteins, and carbohydrates. The Flynn lab studies a hybrid molecule that we discovered called glycoRNA, which is a conjugate of RNA and carbohydrates (glycans). Unlike other RNA species, glycoRNAs are found on the surface of living mammalian cells which places them in an exciting position to control biological processes such as cell-cell communication, host-pathogen interactions, or cell signaling. In the lab, we develop chemical tools and molecular strategies to detect, characterize, and define the functions of glycoRNAs across a range of biological contexts and conditions. Our long-term goal is to control glycoRNA biology for diagnostic and therapeutic benefit.
Christopher Barnes +
Stanford University

Christopher Barnes

Assistant Professor; Biology; Structural Biology

Ph.D., University of Pittsburgh, School of Medicine

M.A., University of North Carolina at Chapel Hill

B.S., University of North Carolina at Chapel Hill

Viruses are inextricably linked to the host cells that they infect. Thus, investigating viral-host interactions is essential to understanding the mechanisms of viral entry, replication, pathogenesis, and the host’s ability to respond to viral pathogens. The Barnes lab excels in leveraging interdisciplinary approaches to address fundamental principles of viral-host interactions for therapeutic benefit. We combine biophysical and structural methods with in vivo approaches to understand how enveloped viruses infect host cells and elicit immune responses. In particular, our research translates knowledge of the structural correlates of antibody-mediated neutralization into the development of highly effective immunotherapies. Additionally, we seek to identify conserved epitopes on viral glycoproteins that are recognized by neutralizing antibodies to facilitate structure-based immunogen design for candidate vaccines against coronaviruses and HIV-1. By combining structural information and improved biochemical methods to mask distracting epitopes, we believe pan-neutralizing vaccines that protect against emerging and re-emerging viral threats are attainable.
Ahmed Abdelfattah +
Brown University

Ahmed Abdelfattah

Robert J. and Nancy D. Carney Assistant Professor of Neuroscience

Ph.D., University of Alberta

B.S., German University of Cairo

Brain circuits are dynamic networks of neurons that process information in the form of electrical and chemical signals to form memories and behaviors. To investigate how brain circuits instantiate fundamental computations underlying behaviors, we need to map their wiring diagrams coupled with functional analysis at cellular resolution to correlate neuron activity with behavior. However, the electrical and chemical signals are not directly visible since there is no natural contrast mechanism that allows us “to see” those signals. The Abdelfattah lab is developing novel classes of molecular tools for large-scale functional analysis and manipulation of brain circuits. In the lab, we repurpose proteins found in nature and engineer them to illuminate brain communication. We hope to use our new molecular tools to unravel the functional basis and causes of neural disorders at a level of detail that has not been accessible to date and empower us to develop novel treatments.
Kevin Monahan +
Rutgers, The State University of New Jersey

Kevin Monahan

Milton E. Cassel Scholar

Assistant Professor; Department of Molecular Biology & Biochemistry

Ph.D., Harvard University

B.S., Haverford College

Kevin Monahan has been designated the Milton E. Cassel Scholar for the 2022 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

In order to fit the long DNA molecules that encode our genome into a tiny nucleus, our cells fold the DNA into complex 3-dimensional structures. This folding does more than save space; it also affects how genes are turned on and off. Intriguingly, different types of cells in the nervous system exhibit distinct 3D nuclear structures. However, the functional significance and regulation of these 3D nuclear structures remains poorly understood. The Monahan lab studies the protein machinery that controls the 3D positioning of genes within the nucleus and how the formation of 3D nuclear structures regulates gene expression. For example, we recently discovered that olfactory sensory neurons, which detect chemical odorants in the air, use the 3D positioning of odorant receptor genes in the nucleus to control the specific type of odorant receptor that they will express. Using molecular, genetic, and genomic approaches, we are investigating protein complexes that regulate 3D nuclear structures in olfactory neurons and in defined populations of neurons within the central nervous system.

2021

Aaron Mickle +
University of Florida

Aaron Mickle

Assistant Professor, Physiological Sciences

B.S., University of Wisconsin – La Crosse

Ph.D., University of Iowa

In conjunction with Margaret and Will Hearst

Chronic pain affects millions of people in the United States, and its socioeconomic burden is currently unprecedentedly high due to the opioid crisis. Almost everyone has either experienced chronic pain or had a family member affected by it. For these reasons, the Mickle lab is passionate about pain research and discovering new therapeutic options for chronic pain patients. Our lab uses a “cell to model organism” strategy to pursue the goal of understanding and delineating the causes of bladder pain dysfunction. We have multiple avenues of research that support this end goal: 1) Pursuing the development of neuromodulation strategies to alleviate bladder dysfunction following spinal cord injury, 2) Evaluating the role of urothelial cells, the cells that line the bladder, in bladder pain and dysfunction, and 3) Developing implantable biosensor and neuromodulatory technology to study bladder disorders and pain.
Nicole Scheff +
University of Pittsburgh

Nicole Scheff

Assistant Professor, Neurobiology

Ph.D., University of Pittsburgh

Head and neck squamous cell carcinoma causes severe pain, increased stress, and reduced quality of life, which exceeds the levels seen in other cancers. Beyond sensory/pain signaling, the peripheral nervous system has been identified as a component of the cancer microenvironment and may be involved in modulating tumor progression and tumor-associated immunity. The cancer microenvironment is comprised of stromal cells, glial cells, immune cells, neurons, (e.g., motor, sensory, sympathetic) and proliferating tumor cells. The Scheff lab seeks to integrate the neurobiology, cancer biology, and immunology fields in order to fully appreciate neural-immune-cancer communication and develop a more holistic approach to novel cancer pain treatment. The goal of my research is to understand how peripheral neurons evolve and adapt during cancer initiation and growth, and to investigate whether therapy targeted to neurons innervating the cancer can alleviate pain and slow tumorigenesis.
Gwendolyn Hoben +
Medical College of Wisconsin

Gwendolyn Hoben

Assistant Professor, Plastic Surgery; Cell biology, neurobiology, and anatomy

Ph.D., Rice University

M.D., Baylor College of Medicine

In conjunction with Margaret and William R. Hearst III

A truly new way to approach a problem surgically is rare and that is what has made targeted muscle reinnervation so fascinating. The unexpected observation that TMR could prevent and reduce residual limb and phantom limb pain in amputees has already impacted the lives of hundreds of patients. The Hoben laboratory has taken TMR from the bedside back to the bench to better elucidate how surgically rearranging nerves affects pain pathways. These changes in nerve connections alter neurons, the fundamental cells of the nervous system. Characterizing the changes in these cells may help identify critical components of residual and phantom limb pain that can be targeted for pain relief. Ultimately, we hope that by better understanding the foundation of TMR pain relief we will be able to apply TMR principles to amputees with chronic pain and other forms of nerve injuries.
Gregory Corder +
University of Pennsylvania

Gregory Corder

Assistant Professor, Psychiatry, Neuroscience

B.S., Tulane University

Ph.D., University of Kentucky

The mission of the Corder Lab at the University of Pennsylvania aims to decipher the neural basis of how the brain generates the perception of pain, and how pathological dysfunction within these brain networks promotes the transition to chronic pain and drug abuse. Using advanced in vivo imaging of neural activity, neuroanatomical tracing, and optical neuromodulation techniques, our group deconstructs the brain circuits and molecular mechanisms involved in pain and emotion. From these basic science investigations, we work collaboratively with others—chemists, bioengineers, and clinician-scientists—to identify translational targets for the development of novel therapeutics that reduce mental health disorders associated with chronic pain and decrease the reliance on prescription opioids.
Viviana Risca +
The Rockefeller University

Viviana Risca

Assistant Professor; Biochemistry, Biophysics, Chemical Biology, and Structural Biology

B.S., Stanford University

Ph.D., University of California, Berkeley

In order to fit into our cells, the human genome is packaged by proteins that protect it from breaks and cancer-causing mutations. These proteins also help cells maintain cell identity by suppressing expression of genes that belong to other cell types. The Risca lab is studying one such protein, called macroH2A, which has been shown to suppress several types of cancer. I recently developed a cutting-edge method for mapping the folding of DNA within cells. We are using this method in combination with biochemical studies of DNA wrapped around purified proteins to study the structural mechanisms that macroH2A uses to regulate gene expression. MacroH2A also interacts with PARP1, a major cancer drug target involved in DNA repair and regulation of transcription, and we hope that these insights will inform future innovations in targeted therapy.
Guosong Hong +
Stanford University

Guosong Hong

Assistant Professor, Materials Science and Engineering

B.S., Peking University

Ph.D., Stanford University

Research from the Hong lab aims to study how the brain changes at the level of single neurons over time as well as the circuits encompassing these neurons. The brain is a dynamically changing structure. The time-dependent evolution of neural circuits during brain development—learning and memory, and aging—occurs over many years and in many different brain regions. However, this evolution involves physiological changes that must be quantified at the millisecond and micrometer scales of individual neurons. A substantial challenge in understanding the dynamically changing brain arises from the spatiotemporal mismatch between the neural activity of interest and the available tools to study it. Therefore, we aim to fill the knowledge gap by developing novel bioelectronic and biophotonic tools to study the long-term evolution of neural circuits during neurodegeneration. The knowledge obtained therein will offer therapeutic strategies for devastating diseases such as Alzheimer’s, thereby improving life quality for the families affected and society as a whole.
Ellen Foxman +
Yale University

Ellen Foxman

Assistant Professor, Laboratory Medicine and Immunobiology

B.S., Yale University

Ph.D., Stanford University School of Medicine

M.D., Stanford University School of Medicine

Our first line of defense against harmful infections is known as innate immunity—an inborn system of protective mechanisms that guards against harmful viruses or bacteria, even when the body has never encountered the infection before. Many individuals infected with dangerous viruses such as influenza or coronavirus can recover quickly with only mild symptoms, even without immunity from prior exposure or vaccination, because of these defenses. The Foxman lab studies the biology of innate immune responses in tissues that are not traditionally considered part of the immune system, such as the cells that form the lining of the nasal passages and lung airways. Understanding how innate immunity is regulated in these tissues could help answer unsolved questions in infectious diseases—why the same viral infection can be asymptomatic in one person, but lead to a serious illness in another; or, on a larger scale, why certain viruses spread through families or communities at certain times but not others.
Lucas Cheadle +
Cold Spring Harbor Laboratory

Lucas Cheadle

Assistant Professor

B.A., Smith College

Ph.D., Yale University

The brain is one of the most exquisitely complex networks in the known universe, and its precise connectivity is established through a convergence of genetic and environmental influences (i.e., nature and nurture, respectively). While many of the genetic factors that drive early stages of embryonic brain development are known, we still lack a comprehensive understanding of how the environment—in the form of sensory experiences—shapes neural circuits in the developing brain. We unexpectedly discovered that sensory experiences engage microglia, a unique class of brain-resident immune cells, to promote the refinement of synaptic connections between neurons early in postnatal life. Based upon this finding, the Cheadle lab combines functional, structural, and genomics approaches to systematically disentangle the mechanisms microglia and neurons use to interact with one another to facilitate postnatal brain development, and to understand how impairments in microglial function contribute to neurodevelopmental disorders.
Joshua Modell +
Johns Hopkins University

Joshua Modell

Assistant Professor, Department of Molecular Biology and Genetics

B.S., Duke University

Ph.D., Massachusetts Institute of Technology

Joshua Modell has been designated the Milton E. Cassel Scholar for the 2021 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

CRISPR technologies have led to revolutionary new modes of genetic inquiry in the basic sciences, and they are in development as therapeutics for many genetic diseases. Less is known about how CRISPR systems function in nature, where they provide bacteria with adaptive immunity against viruses and plasmids. The Modell Lab seeks to understand how these systems interact with the biology of their bacterial hosts and viral targets, and how their activity is regulated to provide strong immunity against viruses while preventing autoimmunity.

2020

Ishmail Abdus-Saboor +
Columbia University (University of Pennsylvania)

Ishmail Abdus-Saboor

Mitchell J. and Margo K. Blutt Presidential Assistant Professor, Biology

B.S., North Carolina A&T University

Ph.D., University of Pennsylvania

In conjunction with Open Philanthropy

My research focuses on a long-standing question—how does the nervous system encode a soft gentle caress versus a harsh painful stimulation? To accomplish this, the Abdus-Saboor Lab uses neurobiology, computational biology, and mathematics to objectively measure pain—a sensory experience that is inherently subjective. Traditionally, researchers have applied sensory stimuli to the rodent paw and tried to infer the animal’s pain state based on the singular readout of whether the animal moved its paw or not. The problem is, animals will lift their paw to both innocuous and noxious stimuli; and with that sole measurement parameter, there is a high likelihood of incorrectly assigning the animal’s sensory experience. An innovation in our work is to use videography to take thousands of images per second to measure sub-second pain behaviors, and couple this with statistical modeling and machine learning to develop rodent “pain scales.”
Grace Chen +
Yale University

Grace Chen

Assistant Professor, Immunobiology

B.S., University of California, Berkeley

Ph.D., Harvard University

An essential function of the immune system is to distinguish between its own and foreign molecules in order to destroy pathogens while preventing destruction of healthy cells. The Chen Lab investigates how the immune system correctly identifies pathogens when the same signals are found in both host cells and pathogens. Circular RNAs (circRNAs)—single-stranded RNAs where the ends are joined together—are encoded by eukaryotes and viruses. We study the essential features of viral and host circRNAs that are required in the regulation and recognition of self- versus non-self, the proteins involved in this process, and the ensuing cellular signaling. We strive to apply our understanding to engineer circRNAs as a novel strategy for immunotherapy that exploits the uniquely promising characteristics of circRNAs.
Geoffroy Laumet +
Michigan State University

Geoffroy Laumet

Assistant Professor, Physiology

Ph.D., Lille University School of Medicine, France

The Laumet Lab is interested in understanding why pain becomes chronic and how can we stop it. While it is obvious that neurons convey pain signaling throughout the body, neurons do not work in isolation and are constantly communicating with and getting influenced by other cells. We are particularly interested in the contribution of non-neuronal cells to chronic pain. We think that impaired communication between “pain-sensing” neurons and their surrounding cells may result in chronic pain. For example, we have discovered that anti-inflammatory molecules secreted by cells from the immune system prevent pain-sensing neurons from becoming persistently activated—this constant activity is the cellular basis of chronic pain. We hope that a better understanding of neuron/non-neuronal cell communication will lead to the development of new and better analgesics.
Sarah Linnstaedt +
University of North Carolina at Chapel Hill

Sarah Linnstaedt

Assistant Professor, Anesthesiology

B.S., Virginia Tech

Ph.D., Georgetown University

In conjunction with Open Philanthropy

Almost all individuals will experience at least one traumatic injury in their lifetime. While the majority of these individuals recover, a substantial subset develop chronic post-traumatic pain (CPTP). The Linnstaedt Lab is interested in better understanding how to predict which individuals will recover versus develop CPTP following trauma, and how to prevent CPTP in those at high risk. To address this goal, we use translational research approaches to discover genetic and molecular vulnerability factors that predict CPTP and to identify promising targets for therapeutic preventative interventions.
Jeremy M. Rock +
The Rockefeller University

Jeremy M. Rock

Assistant Professor, Microbiology and Infectious Diseases

B.A., University of California, Berkeley

Ph.D., Massachusetts Institute of Technology

Mycobacterium tuberculosis is the leading cause of death due to infectious disease and it infects one-quarter of the world’s population. By investigating the mechanisms that enable this bacterium to cause tuberculosis and evade current antibiotics, the Rock Lab aims to lay the foundation for new therapeutic strategies to improve control of this epidemic.
Andrew J. Shepherd +
The University of Texas MD Anderson Cancer Center

Andrew J. Shepherd

Assistant Professor, Department of Symptom Research

B.S., The University of Manchester Institute of Science and Technology, United Kingdom

Ph.D., The University of Manchester, United Kingdom

Work in the Shepherd Lab focuses on how injury, inflammation, and cancer interact with the nervous system to cause pain. We are particularly interested in how chronic illnesses disrupt the immune system, thereby increasing pain risk. Macrophages, a type of immune cell, are important contributors to pain. Macrophages infiltrate damaged tissue to clear debris and infection. Ordinarily, this process eventually resolves, promoting healing. We hypothesize that chronic pain often stems from macrophages failing to make this transition from a “damage response” to a “pro-repair” state. In such cases, macrophages continually sustain inflammation, causing nearby nerves to remain hyper-excitable and drive chronic pain. Our knowledge of these mechanisms is surprisingly limited, a problem that is set to become more widespread as chronic illnesses and cancer survivorship improve. We hope that improving our understanding of these “neuro-immune” interactions will identify novel therapeutic targets and facilitate the development of safe and effective analgesics.
Tuomas Tammela +
Memorial Sloan Kettering Cancer Center

Tuomas Tammela

Assistant Member

M.D., University of Helsinki, Finland

Ph.D., University of Helsinki, Finland

Cancer cells within tumors assume distinct identities, forming diverse cellular societies. Despite this diversity, the current paradigm is to treat tumors with homogeneous cancer therapy regimens. This thinking persists despite strong evidence from preclinical models and human patients that tumors are heterogeneous and, therefore, cellular identities capable of withstanding and adapting to therapies invariably exist. The Tammela Lab seeks to understand how cancer cells acquire the ability to transition between these identities and promote intra-tumoral heterogeneity. To do this, we will use a series of innovative approaches and models of human cancer. Our hope is that these efforts will lead to conceptually new types of cancer therapies to prevent cancer cells from transitioning to treatment-resistant states.
David Van Valen +
California Institute of Technology

David Van Valen

Assistant Professor, Biology and Biological Engineering

B.S., Massachusetts Institute of Technology

M.D., University of California, Los Angeles

Ph.D., California Institute of Technology

Viruses are in constant conversation with the cells they infect, and the information exchanged can be used by the host or the virus to guide their respective behaviors. For example, viruses may decide to become dormant after infection, while host cells may choose to activate an immune response. The Van Valen Lab listens in on this conversation to understand how viruses and their hosts represent information about their internal state and their environment, and how this information is accessed to make decisions. To do so, we combine ideas from cell biology and physics with recent advances in imaging, machine learning, and genomics to make novel measurements of host–virus interactions. Active projects include imaging the interaction between host immune and metabolic signaling networks during infection, measuring host–virus interactions in a model system of viral latency, and developing novel deep-learning approaches to single-cell analysis of biological imaging data.
Amanda Whipple +
Harvard University

Amanda Whipple

Assistant Professor, Molecular and Cellular Biology

B.S., The University of Oklahoma

Ph.D., Baylor College of Medicine

Amanda Whipple has been designated the Milton E. Cassel Scholar for the 2020 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

Our DNA represents the full library of genetic information each of us inherits from our parents. We inherit two copies of each gene—one from our mother and one from our father. Typically, the two copies are treated equally in the cell. However, the Whipple Lab studies a unique class of “imprinted genes,” in which only one parental copy is active (“expressed”) while the other is inactive (“silenced”). Many imprinted genes are expressed in the brain and are associated with diverse neurological disorders. Yet, the reasons for imprinted expression and the effects of imprinted gene activity in the brain remain largely unknown. We use molecular and bio-computational approaches to understand: (1) why genes evolved imprinted expression in the brain, (2) how imprinted genes function in neurons, and (3) how dysregulation of imprinted genes contributes to neurological diseases.

2019

Li Zhao +
The Rockefeller University

Li Zhao

Assistant Professor, Evolutionary Genetics and Genomics

B.S., Inner Mongolia University, China

Ph.D., Chinese Academy of Sciences

Each living species and every phylogenetic clade has a unique set of genes and phenotypes. Understanding how novel genes originate and subsequently evolve is crucial to explaining the genetic basis of novel phenotypes and ultimately the diversity of life. However, because the relationship between genes and phenotypes is complex and multidimensional, how and what type of genetic innovations contribute to novel organismal phenotypes remains largely unknown. Research in the Zhao Laboratory aims to understand the origination and evolution of molecular innovations as well as how they contribute to phenotypic innovation and adaptation. One of the focuses in the lab is to use de novo genes, which are genes that have originated from non-genic sequences of genomes, as a unique paradigm to tackle these questions. In the long-term, the Zhao lab aims to decipher the principles of gene origination and its underlying positive or negative impact on population dynamics and human health.
Vivianne Tawfik +
Stanford University

Vivianne Tawfik

Assistant Professor, Anesthesiology, Perioperative, and Pain Medicine

B.Sc., McGill University

M.D./Ph.D., Dartmouth College

In conjunction with the Open Philanthropy Project

The mission of the Tawfik Lab is to do the best clinically informed basic science research to advance our understanding of the neuroimmune contribution to chronic pain in a thoughtful manner, with our patients always in mind. We are particularly interested in understanding the unique underpinnings of various types of chronic pain and how central nervous system glial cells (astrocytes and microglia) contribute to the transition from acute to chronic pain. Microglia are particularly interesting to us, as the macrophages of the central nervous system with known roles in synaptic pruning and neuroinflammation. Funding from the Open Philanthropy Project will allow us to dive more deeply into the contribution of spinal cord microglia using transgenic manipulations and microglial transcriptome analyses in a mouse model of complex regional pain syndrome (CRPS), a disease that affects the limbs after minor fracture, or surgery. We expect that our findings in this model will also extend to other forms of chronic pain and allow for the development of more specific glial-targeted therapeutics.
Lauren O’Connell +
Stanford University

Lauren O’Connell

Assistant Professor, Biology

B.S., Cornell University

Ph.D., University of Texas at Austin

Communication of nutritional need during infancy is our very first social interaction, laying the foundation for a healthy life by acquiring nutrition for growth and establishing strong social bonds with caregivers. The O’Connell Lab uses a unique biological model—translucent social tadpoles—to uncover how neonates evaluate their nutritional state, recognize their caregivers, and communicate to their caregivers that they need food. We will carry out this research by mapping the molecular and cellular mechanisms that regulate neonate feeding behavior and social communication of hunger. These studies have implications for informing preventative strategies and treatments for childhood eating disorders and autism spectrum disorders—two of the most prevalent diseases afflicting the youngest members of our society.
Jordan McCall +
Washington University in St. Louis

Jordan McCall

Assistant Professor, Anesthesiology

B.S./B.A., University of Missouri Columbia

M.P.H., University of Missouri Columbia

Ph.D., Washington University in St. Louis

In conjunction with the Open Philanthropy Project

I lead a multidisciplinary research program aimed at understanding the neural mechanisms underlying the emotional distress associated with stress, chronic pain, and addiction. The long-term goal of the laboratory is to use a neural circuit-level understanding of the brain systems that are disrupted in anxiety and chronic pain to reverse these conditions. If these questions become intractable, the laboratory plans to develop new wireless technology to interface with the nervous system and explore new approaches to data analysis to access the most information from collected data.
Meghan Koch +
Fred Hutchinson Cancer Research Center

Meghan Koch

Assistant Member, Basic Sciences Division

B.S., University of California, Santa Barbara

Ph.D., University of Washington, School of Medicine

My lab is interested in understanding how maternal-offspring interactions influence neonatal health. We take a comprehensive approach, analyzing multiple aspects of physiology such as immunity, development, and metabolism. Recently, we demonstrated that healthy mothers produce a range of antibodies that bind to bacteria living in the infant gut. Transfer of these antibodies to offspring through breast milk is necessary to limit neonatal immune responses and promote peace between gut bacteria and their infant hosts. Currently, we are characterizing how these antibodies are generated, exploring how maternal antibodies achieve their effects, and determining the long-term consequences these antibodies have on offspring health. Additionally, we are developing systems to identify and characterize how the complete set of maternal-derived factors contributes to health.
Peter Grace +
University of Texas MD Anderson Cancer Center

Peter Grace

Assistant Professor, Symptom Research

B.S., University of Adelaide

Ph.D., University of Adelaide

In conjunction with the Open Philanthropy Project

Pain that becomes chronic and outlasts the period of healing is a major medical challenge. The Grace Lab investigates the neuroimmune interactions that drive chronic pain. After injury to sensory nerves, glial cells, such as microglia and astrocytes, are activated throughout the central nervous system. These activated glia secrete neurotransmitters and cytokines that increase the excitability of neurons in pain pathways. We are focused on the open question of how spinal cord astrocytes are persistently activated in such remote regions. This line of research is also being expanded to determine how activated glia in the brain also contribute to common comorbidities of chronic pain, including depression, anxiety, and cognitive impairments. The ultimate goal of this work is to find new ways to treat chronic pain.
Meaghan Creed +
Washington University in St. Louis

Meaghan Creed

Assistant Professor, Anesthesiology

B.S., University of Toronto Scarborough

Ph.D., University of Toronto

Our research focuses on synaptic plasticity and neuromodulation within defined neural circuits in the ventral basal ganglia, a collection of brain structures involved in reward learning and selection of flexible behavior. Specifically, we ask how chronic pain, addictive drugs, or genetic mutations alter the function of these neural circuits, and how circuit dysfunction contributes to symptoms of chronic pain, substance use, and mood disorders. Our ultimate goal is to leverage insight from circuit studies to develop novel neuromodulation for these disorders, including deep brain stimulation and focused ultrasound. By first determining how neuronal and circuit adaptations drive specific behavioral symptoms of disease, we can establish a strategy for targeted circuit manipulation in a disease state. We then rationally design neuromodulation paradigms and validate them in model systems to provide novel strategies to treat symptoms at the interface of chronic pain, mood, and substance use disorders.
E. Josie Clowney +
University of Michigan

E. Josie Clowney

Assistant Professor, Molecular, Cellular, and Developmental Biology

B.S., University of Michigan

Ph.D., University of California, San Francisco

Josie Clowney has been designated the Milton E. Cassel Scholar for the 2019 class of Rita Allen Foundation Scholars. This special award honors the memory of a longtime President of the Rita Allen Foundation who passed away in 2004.

Our bodies make direct contact with environment-derived molecules including volatiles, dietary nutrients, and microbial components. The evolutionary problem of detecting and responding to extraordinarily diverse exogenous compounds has been solved similarly in chemosensory, digestive, and immune systems, by the evolution of large families of cell surface and secreted proteins whose members each have limited binding affinities. The Clowney lab studies how these large gene families evolved; how they are coordinately regulated across cells; and, in the chemosensory system, how signals flowing through chemosensory receptors can be meaningfully interpreted to allow suitable behavioral responses. We are particularly interested in understanding the distinct biological mechanisms that allow reflexive responses to evolutionarily predicted stimuli versus flexible responses to arbitrary or evolutionarily unpredicted stimuli.
Michael Burton +
University of Texas at Dallas

Michael Burton

Assistant Professor, Behavioral and Brain Sciences

B.S., University of Illinois at Urbana-Champaign

Ph.D., University of Illinois at Urbana-Champaign

Recent initiatives have revealed the importance of how different cell types recognize and respond to pain stimuli. Mastering these single-cell paradigms will lead to a better understanding of mechanisms in pain plasticity and evolve new therapeutics. My work sits at an important interface between the immune and nervous system and strives to understand the complex nature of their interconnectivity. The lab has three areas of focus: inflammation, aging, and cannabinoid signaling. We hope to understand how factors like age, sex, and endogenous cannabinoid signaling modulate pain outcomes.
Matthew Banghart +
University of California, San Diego

Matthew Banghart

Assistant Professor, Neurobiology

B.S., University of the Sciences in Philadelphia

Ph.D., University of California, Berkeley

Our perception of the world around us is heavily shaped by factors such as prior experience, expectations, attentional focus, and drugs—both therapeutic and recreational. Yet, how context influences sensory information processing in the brain is largely a mystery. The Banghart Lab aims to understand how the brain controls the perception of pain. Toward this goal, the lab studies the neural mechanisms that support both pharmacological analgesia (e.g. opioid painkillers), as well as “top-down” pain modulation, wherein pain suppression is driven purely by cognitive processes (e.g. placebo analgesia). By revealing the similarities and differences between the neural circuits and neurochemical signals that underlie these forms of pain modulation, this work may one day contribute to the development of new therapies.

2018

Helen Lai
The University of Texas Southwestern Medical Center
Paul Greer
University of Massachusetts Medical School
Candice Paulsen
Yale University
Lindsay Schwarz
St. Jude Children’s Research Hospital
Joseph Parker
California Institute of Technology
Vincent Luca
Moffitt Cancer Center
Emily Hatch
Fred Hutchinson Cancer Research Center

2017

Dingding An +
Boston Children’s Hospital

Dingding An

Research Associate, Boston Children’s Hospital
Assistant Professor of Pediatrics, Harvard Medical School

B.S., Environmental Science and Engineering, Tsinghua University
M.S., Environmental Engineering, Duke University
Ph.D., Environmental Engineering and Microbiology, Northwestern University

Project: How do signals from resident bacteria keep the intestines healthy?

Motivated by a desire to advance strategies for environmental protection, Dingding An began her undergraduate education in environmental engineering at Tsinghua University in Beijing. She took many courses in chemistry and physics, but was increasingly drawn to biology. An’s research experience at Duke University helped her make this transition—she chose a laboratory that focused on the remediation of pollution by microbial processes, and discovered she had a keen interest in working with bacteria.

In her doctoral research, An explored how multiple species of bacteria grow, survive and compete in communities called biofilms, which are known for posing problems in food production and medicine. During the course of her Ph.D., she followed her mentor, Matthew Parsek, from Northwestern University to the University of Iowa, and finally to the University of Washington School of Medicine in Seattle. This exposure to diverse biological research environments inspired An to pursue research on host-microbe interactions.

As a postdoctoral fellow in Dennis Kasper’s lab at Harvard Medical School, she began using mouse models to examine microbes that function not as pathogens, but as partners. She studied how bacteria living in the intestine modulate the immune system and protect the host from inflammatory bowel disease. An found that this protection is conferred in part by unique yet abundant bacterial molecules called sphingolipids. Now, An and her team are seeking a fuller understanding of sphingolipids in intestinal health. Their research will address why these bacterial signals seem to be important early in life, and how sphingolipids affect the production of mucus, which forms a critical barrier between bacterial cells and the host’s intestinal cells. “Eventually, I think we could identify specific sphingolipids produced by bacteria and use them as therapeutics to specifically help patients when they have a mucus production problem,” she says.
Kyle Baumbauer +
The University of Kansas (University of Connecticut School of Nursing)

Kyle Baumbauer

Kyle Baumbauer (Award in Pain Recipient) earned a B.S. in psychology and a B.A. in sociology from the University of Central Florida. He holds an M.A. and Ph.D. in experimental psychology from Kent State University, where he studied molecular mechanisms that allow neurons in the spinal cord to mediate learning and adaptation to the environment. This research contributed to an emerging view of the spinal cord not merely as a channel for signals traveling to and from the brain, but as a dynamic group of nerves with important effects on behavior. Baumbauer continued this area of research while a postdoctoral fellow at Texas A&M University, and explored how painful stimulation impacts spinal cord function to understand how the presence of pain affects the recovery of function after spinal cord injury. Baumbauer then did a second fellowship at the University of Pittsburgh, where he began examining the impact of injury and inflammation on peripheral sensory neuron function.

In 2014 Baumbauer joined the faculty at the University of Connecticut School of Nursing, where his research focuses on unraveling the relationship between alterations in gene expression and sensory neuron function, and how these processes contribute to chronic pain following spinal cord injury. Through these investigations, Baumbauer and his team aim to make advances that aid in the treatment of pathological pain. In addition to the Rita Allen Foundation Baumbauer’s research is supported by the National Institute of Neurological Disorders and Stroke. He is also a recipient of a Mary Lawrence Research Development Award from the UConn School of Nursing and has been honored as a Sigma Theta Tau Friend of Nursing.
Richard Daneman +
University of California, San Diego

Richard Daneman

Richard Daneman has been designated the Milton E. Cassel Scholar for the 2017 class of Rita Allen Foundation Scholars. This special award honors the memory of a long-time President of the Rita Allen Foundation who passed away in 2004.

Assistant Professor of Neuroscience and Pharmacology

B.Sc., Biochemistry, McGill University
Ph.D., Developmental Biology, Stanford University

Project: How does the blood–brain barrier influence the activities of neurons in the brain?

Richard Daneman grew up in an academic family. His parents, a cognitive psychologist and a pediatric endocrinologist, sometimes enlisted him and his brother to serve as research subjects. From an early age, Daneman says, he was attracted to the “amazing adventure” of science: “I loved asking a question that had no answer and trying to work out different ways that you could solve a problem.” As an undergraduate, he got involved in projects to develop new laboratory techniques—to measure fine-scale pH changes within cells, and to analyze gene expression patterns in fruit flies.

Daneman conducted graduate work at Stanford University with Ben Barres, a neurobiologist known for research on glial cells, which make up a large proportion of cells in the nervous system but are vastly understudied. The Barres lab was an ideal setting for Daneman to pursue another overlooked aspect of the nervous system: the blood–brain barrier. He led studies to identify molecular signals that give blood vessels in the central nervous system their unique properties—unlike the “leaky” blood vessels in other tissues, they restrict the movement of toxins, pathogens and immune cells.

Daneman continued to focus on the blood–brain barrier during a fellowship at the University of California, San Francisco, and is now pursuing multiple questions related to the barrier’s development and its breakdown in conditions of injury or disease. He recently discovered physiological processes within the brain’s blood vessels that could influence the function of neurons. The Rita Allen Foundation award will allow Daneman and his team to examine the role of the blood–brain barrier in brain functioning. “We think of blood vessels as these tubes that run through the brain,” he says. “But the idea that they have these dynamic physiological properties that can fine-tune and manipulate the [neural] circuits—we know nothing about that.”
Arkady Khoutorsky +
McGill University

Arkady Khoutorsky

Arkady Khoutorsky (Award in Pain Recipient) earned a B.Sc. in biology and an M.Sc. in neurobiology, as well as D.V.M. and Ph.D. degrees, from the Hebrew University of Jerusalem. During a postdoctoral fellowship at McGill University, Khoutorsky investigated how regulation of protein synthesis controls neuronal plasticity in the brain and in the pain pathway. He joined McGill’s Alan Edwards Centre for Research on Pain in 2016. In addition to the Rita Allen Foundation, Khoutorsky’s work is supported by the Canada Foundation for Innovation, and by a NARSAD Young Investigator Grant and a Louise and Alan Edwards Foundation Grant in Chronic Pain Research.

Khoutorsky’s lab is examining how neuronal circuits in the spinal cord are remodeled to promote sensitivity to pain. He is interested in the extracellular matrix, a network of proteins that surrounds neurons. In the brain, this matrix appears to restrict the ability of neurons to form the new structures necessary for learning and memory. Enzymes that degrade the matrix are activated in some chronic pain conditions. Khoutorsky and his team are investigating how such degradation impacts spinal cord neurons that normally inhibit pain signals. They aim to determine how changes in the extracellular matrix might enable the neurons to become “hyperexcitable” and inappropriately propagate pain.
Stephan Lammel +
University of California, Berkeley

Stephan Lammel

Assistant Professor of Neurobiology

B. Pharm., Philipps-University, Marburg, Germany
M.Sc., Neuroscience, Martin-Luther-University, Halle, Germany
Ph.D., Neuroscience, Philipps-University, School of Medicine, Marburg, Germany

Project: How can chronic stress change neural circuits and lead to depression?

Stephan Lammel has a longstanding interest in medicine, and began training as a pharmacist with the intention of taking over his family’s business. During his pharmacy residency, he grew frustrated with the limitations and side effects of currently available medications—particularly for neurological disorders such as Parkinson’s disease and schizophrenia. Then he met a researcher, Jochen Roeper, who was studying how dopamine neurons degenerate in Parkinson’s disease.

Lammel was excited by the opportunity to explore the underlying neurobiology of the dopamine system, and to make discoveries that could guide more effective therapeutic approaches. He joined Roeper’s lab as a master’s student, and later pursued a Ph.D. His work helped to reveal diversity in the properties of dopamine-containing neurons. As a postdoctoral scholar in Robert Malenka’s lab at Stanford University, Lammel continued investigating dopamine neurons, including neural circuits involved in reward and motivation.

With support from the Rita Allen Foundation, Lammel and his team will apply new technologies to examine the mechanisms by which chronic stress can lead to depression. Better knowledge of these mechanisms is crucial to treating depression, he says, as today’s outdated therapies are effective for less than half of patients, and have many undesirable side effects. Lammel’s research group will follow changes in neural activity in freely moving animals over time, using methods such as optogenetics and in vivo calcium imaging to visualize changes in activity among specific populations of neurons. “If we understand the circuits in which these neurons are embedded, we can manipulate them in a more specific way and try to reverse some of the pathological changes in these circuits”, he explains. “Ultimately, we hope these manipulations can also reverse some of the symptoms of depression.”
Conor Liston +
Weill Cornell Medicine

Conor Liston

Assistant Professor of Neuroscience and Psychiatry, Feil Family Brain and Mind Research Institute

A.B., Psychology and Biology, Harvard College
Ph.D., Neuroscience, The Rockefeller University
M.D., Weill Cornell Medicine

Project: What are the molecular mechanisms of working memory?

As an undergraduate, Conor Liston became fascinated by the science of learning and memory, and by larger questions of how the brain gives rise to consciousness. “One of the things that attracted me to neuroscience was the potential for discoveries that would transform the way we think about ourselves as people, and also could potentially transform the way we think about diagnosing and treating disorders of the brain,” he says.

Liston’s desire to improve the understanding and treatment of mental illness led him to pursue an M.D.-Ph.D. During his psychiatry residency at NewYork-Presbyterian/Weill Cornell Medical Center, he also conducted postdoctoral research with Wen-Biao Gan at New York University, investigating how stress hormones affect neural connections critical for learning. This research fueled his interest in new technologies for visualizing and experimentally manipulating activity in the living brain, and led him to a fellowship at Stanford University. There, Liston worked in the laboratory of Karl Deisseroth, known as a pioneer of optogenetics—a technique for controlling and monitoring neurons using specific wavelengths of light. Liston used optogenetics and other new imaging methods to explore the neural circuitry of fear responses and reward-seeking behaviors.

Now, Liston, an assistant professor of neuroscience in the Feil Family Brain and Mind Research Institute, treats psychiatric patients in the clinic, and leads a research program on the neuroscience of learning, memory, stress and depression. Support from the Rita Allen Foundation will allow Liston and his team to investigate the basis of working memory—the type of memory that operates when we remember and call a phone number, but forget it a few hours later. Working memory “is both stable and robust enough to not be interfered with by irrelevant information in our environment, but also labile enough to be easily deleted and replaced with new information,” Liston explains. “That’s an interesting paradox: How does our brain register memories that have these two competing qualities?” He plans to examine how different subtypes of neurons interact to achieve this balance—and how it can be disrupted in conditions such as depression.
Kate Meyer +
Duke University School of Medicine

Kate Meyer

Assistant Professor of Biochemistry

B.S., Biopsychology and Cognitive Sciences, University of Michigan
Ph.D., Neuroscience, Northwestern University

Project: How does a modification of RNA influence the brain’s development and activity?

As a child, Kate Meyer had ambitions of becoming a surgeon, and entered college on a premedical track. A course on abnormal psychology fueled her fascination with the brain’s complexity, and she switched her focus to neuroscience. She helped with a research project on the neural basis of taste, which involved “scoring rat behaviors for hours on end, and loving it,” she recalls. “I was super excited to do literally anything” in the laboratory, Meyer adds.

She sought further training in neuroscience as a Ph.D. student in Jill Morris’ lab at Northwestern University, where she investigated the expression pattern of a gene implicated in schizophrenia and assessed its role in the developing brain. During a postdoctoral fellowship with Samie Jaffrey at Weill Cornell Medical College, Meyer delved into the biology of RNA. She led a comprehensive analysis of an RNA modification called m6A—the methylation of adenosine residues, a chemical marker that can influence whether an RNA molecule is translated into protein. Using next-generation sequencing, Meyer and her colleagues showed that the modification is widespread among thousands of genes in mammals, and that its prevalence increases in the brain during development.

In her own laboratory at Duke, Meyer and her team are exploring how the m6A modification affects when and where genes are expressed—with special attention to how this regulation shapes the growth, connections and activities of neurons. Her goal, she says, is “to understand, all the way from the molecular level to the behavioral level, what happens if we manipulate this pathway that controls methylation. What are the consequences for things like learning and memory, or neurological disease?”

2016

Steve Davidson +
University of Cincinnati College of Medicine

Steve Davidson

Steve Davidson (Award in Pain Recipient) earned a B.S. in psychology from the University of New Orleans and a Ph.D. in neuroscience from the University of Minnesota. He was a postdoctoral scholar in the Department of Anesthesiology at Washington University School of Medicine in St. Louis from 2009 to 2014, and in 2015 he joined the faculty of the University of Cincinnati College of Medicine. In 2010, Davidson received a Future Leader in Pain Research award from the American Pain Society.

Pain has long been recognized as a multidimensional experience. Yet research has focused almost exclusively on the sensory dimension, leaving the emotional and motivational components poorly understood and undertreated. The Davidson lab seeks to elucidate and control a neural circuit responsible for regulating the capacity for pain tolerance, an aspect of pain behavior dependent on emotional and motivational pain processing that occurs in the brain. Davidson’s research tests the main hypothesis that effective pain control can be achieved by manipulating neural activity in a thalamo-limbic pathway to enhance pain tolerance. His laboratory has developed a novel operant behavioral model in which rodents may obtain a reward by engaging with (tolerating) a noxious thermal stimulus. Using this approach, analgesics with efficacy for improving the affective measure of pain tolerance vs. reflexive withdrawal may be determined. To determine whether thalamo-limbic projection neurons control pain, virally infected posterior thalamic neurons containing optically gated ion channels will allow direct control of activity through an implanted light source while animals are tested for changes to pain tolerance and reflexive behaviors. Finally, the Davidson lab will test the hypothesis that chronic pain alters synaptic plasticity in the thalamo-limbic circuit. This will include examination of posterior thalamic projection neurons for altered excitability and synaptic plasticity at the posterior thalamus-insula synapse in rodent models of neuropathic and inflammatory chronic pain.
Camila dos Santos +
Cold Spring Harbor Laboratory

Camila dos Santos

Camila dos Santos completed undergraduate, master’s and doctoral studies at the University of Campinas in Brazil. She was a postdoctoral fellow at the Children’s Hospital of Philadelphia, as well as a postdoctoral fellow and research investigator at Cold Spring Harbor Laboratory with Gregory Hannon, a 2000 Rita Allen Foundation Scholar and a member of the Foundation’s Scientific Advisory Committee. She became an assistant professor at CSHL in 2015. In addition to the Rita Allen Foundation award, dos Santos has received a Glen Cove Cares Research Award, a Pershing Square Foundation Scholar Award and a research award from the Manhasset Women’s Coalition Against Breast Cancer.

The dos Santos laboratory aims to uncover the molecular basis of pregnancy-induced breast cancer protection. In humans, a full-term pregnancy before the age of 25 is known to reduce the risk of developing breast cancer by more than one-third. In rodents, pregnancy can decrease the frequency of carcinogen-induced mammary tumors by more than 60 percent. A recent study by dos Santos and colleagues has shown that transitions through pregnancy lead to massive and stable reorganization of DNA methylation in mammary epithelial cells. Now they propose to further characterize this phenomenon by mapping genome-wide enhancer activity in this system. They will test the hypothesis that the parous (post-pregnancy) epigenome modulates the effects of breast cancer oncogenes on epithelial cell oncogenesis. In addition, they will investigate pharmacological strategies that mimic these effects, which may provide a path toward strategies for breast cancer prevention.
Monica Dus +
University of Michigan

Monica Dus

Monica Dus (Milton E. Cassel Scholar) earned a B.S. in biology from the University of Redlands in Redlands, California, and a Ph.D. in the Watson School of Biological Sciences at Cold Spring Harbor Laboratory, where she worked with Gregory Hannon, a 2000 Rita Allen Foundation Scholar and a member of the Foundation’s Scientific Advisory Committee. After a postdoctoral fellowship in Greg Suh’s lab at the New York University School of Medicine, she became an assistant professor at the University of Michigan in 2015. In addition to being a Rita Allen Foundation Scholar, Dus has received a Pathways to Independence K99/R00 Award from the National Institute of Diabetes and Digestive and Kidney Diseases, a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation and a Klingenstein-Simons Fellowship Award in the Neurosciences.

One of the oldest debates in biology is that of nature versus nurture. Are our behaviors dictated by genes or by the environment? In the last decade it has become clear that neuroepigenetic processes play a key role in adult brain function by merging environmental information with ongoing brain processes to direct behavioral states. Disruption in these processes is linked to both normal and abnormal behaviors, such memory and addiction. However, the underlying mechanisms remain mysterious. In particular, we have no knowledge about the genetic loci of integration between the environment and behavior, or the identity of the neural pathways that control them in specific neural circuits. This presents a major roadblock to unlocking the molecular interface between brain and environment and the role it plays in brain function. To understand how the environment shapes and reprograms brain and behavior, the Dus lab exploits: 1) a simple behavior, eating, which is dependent on an experimentally controllable environment, diet; and 2) the fruit fly brain, which is orders of magnitude smaller than vertebrate brains, but shows conserved neurochemistry.
Katherine Hanlon +
Presbyterian College School of Pharmacy (University of New England College of Osteopathic Medicine)

Katherine Hanlon

Katherine Hanlon (Award in Pain Recipient) earned a B.S. in biochemistry and molecular biophysics and a Ph.D. in pharmacology from the University of Arizona, where she worked with Todd Vanderah. She went on to complete a postdoctoral fellowship in tumor immunology at the Mount Sinai Medical Center with Joshua Brody and Peter Heeger. In addition to her work in the lab, Hanlon currently teaches Biochemistry and Principles of Pharmacology in the School of Pharmacy at Presbyterian College and directs the College’s Office of Research. Her primary research interests include macrophage-neuron communication in pain processing and the role of tumor-associated macrophages in cancer development. She also studies the mechanisms of dysregulation of cannabinoid receptor signaling in tumor and immune cells in metastatic disease.

Studies in the Hanlon lab are carried out using multiple in vitro and in vivo models, including leukocytes and neurons isolated from dorsal root ganglia, leukocytes and tumor cells isolated from murine mammary tumors, leukocytes harvested from post-surgical peritoneal adhesions, and human blood monocyte primary cultures. With the support of the Rita Allen Foundation and the American Pain Society, the lab is able to explore the communication that occurs between sensory neurons and macrophages (innate immune cells that are critical in injury response) in dorsal root ganglia (DRG). Macrophages in the DRG are a unique population of cells that bear some resemblance to brain microglia, but are functionally distinct and exhibit specific phenotype differences. In response to peripheral injury, DRG macrophages respond to activity in the ascending pain pathways and may alter pain perception. By evaluating the phenotype and function of this unique population, Hanlon hopes to isolate novel and exploitable mechanisms that may be used to develop non-opioid therapeutics for the treatment of persistent pain.
Alex Kentsis +
Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College

Alex Kentsis

Alex Kentsis received undergraduate and master’s degrees from the University of Chicago, where he conducted research in the laboratory of Tobin Sosnick. He earned a Ph.D. from New York University, where he worked with Katherine Borden, and an M.D. from Mount Sinai School of Medicine, where his advisor was Roman Osman. He completed research and clinical fellowships at Boston Children’s Hospital and the Dana-Farber Cancer Institute, where he later became an attending physician, as well as an instructor at Harvard Medical School. He joined the faculties of Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College in 2013. In addition to being a Rita Allen Foundation Scholar, Kentsis has received a Damon Runyon Cancer Research Foundation Clinical Investigator Award, an American Society for Clinical Investigation Physician-Scientist Award, an American Society of Hematology Scholar Award and a Burroughs Wellcome Fund Career Award for Medical Scientists.

Genome sequencing efforts have revealed a surprising dearth of gene mutations in many human cancers, suggesting that alternative oncogenic mechanisms must be investigated to identify targets for improved therapy. Approximately half of the human genome originates from mobile DNA elements, or transposons, but their contributions to human disease and physiology remain almost completely unexplored. Kentsis aims to investigate mechanisms of tumorigenesis by a novel human DNA transposase in embryonal tumors, lethal childhood cancers that are refractory to intensive chemotherapy. Successful completion of proposed studies promises to transform our ability to identify the drivers of human cancer, thus leading to improved targeted therapies for these refractory pediatric tumors. This work will also establish powerful tools for the investigation of DNA transposition and genomic plasticity, with transformative applications in wide areas of human biology.
Bo Li +
The University of North Carolina at Chapel Hill

Bo Li

RELATED STORY: Foundation Scholars Earn NIH Awards for High-Risk, High-Reward Research

Bo Li earned her B.S. in biological sciences from Beijing University and her Ph.D. in biochemistry from the University of Illinois at Urbana-Champaign. She was a postdoctoral fellow in the Department of Biological Chemistry and Molecular Pharmacology at Harvard Medical School, where she worked with Christopher T. Walsh. She has received a a Jane Coffin Childs Memorial Fund for Medical Research Fellowship and a National Institutes of Health Pathway to Independence Award.

Li’s lab identifies bioactive small molecules produced by bacteria—she and her colleagues explore the chemistry of their production and study the roles they play in the biology of bacteria and human hosts. Bacteria craft these gene-encoded molecules from primary metabolites using complex chemical transformations; the structures and activities of these small molecules have been optimized through millions of years of evolution and enable these molecules to mediate extensive microbe-microbe and microbe-host interactions. Li’s multidisciplinary research program uses bacterial genomics and metabolomics as enabling technologies to identify novel bacterial small molecules. First, her team is identifying small molecules from soil bacteria as novel antibiotics to combat multidrug-resistant pathogens; second, they are identifying metabolites produced by the human gut microbiota to unravel the chemical and molecular mechanisms of bacterial symbiosis and pathogenesis. Her work involves understanding fundamental biosynthetic mechanisms and extends to exploiting bacterial small molecules to improve human health and prevent disease.
Katharina Schlacher +
The University of Texas MD Anderson Cancer Center

Katharina Schlacher

Katharina Schlacher obtained her B.S. in microbiology at the Karl-Franzens University in Graz, Austria. For graduate studies, in 2003 she joined the lab of Myron Goodman at the University of Southern California, where she earned her Ph.D. While there, she discovered an unprecedented transactivation mechanism for mutagenic E. coli DNA polymerase V by proteobacter recombinase RecA, recognized by the USC College Doctoral Research Prize. In 2007, as a Damon Runyon Postdoctoral Fellow, Schlacher joined Maria Jasin at Memorial Sloan Kettering Cancer Center (MSKCC) and Hong Wu at the University of California, Los Angeles, to focus on her passion for mechanisms at the replication fork. She discovered a novel genomic instability and tumor suppressor mechanism at the DNA replication fork distinct from DNA repair. Specifically, Fanconi anemia proteins BRCA1/2 protect stalled DNA replication forks from degradation by MRE11. This replication fork protection discovery was recognized with the Parvin Foundation Award for academic excellence, the UCLA/Molecular Biology Institute Research Excellence Award and the MSKCC Postdoctoral Research Award. Schlacher received a National Cancer Institute K22 award and joined the faculty at MD Anderson Cancer Center in 2014.

Schlacher’s research focuses on developing an in-depth molecular and biological understanding of how replication fork protection suppresses cancer and disease to obtain biological insights suitable to develop disease prevention and treatment strategies.

2015

Minoree Kohwi +
Columbia University

Minoree Kohwi

Minoree Kohwi’s interest in brain development started as an undergraduate in Mark Konishi’s lab at the California Institute of Technology. She earned a Ph.D. in Arturo Alvarez-Buylla’s lab at the University of California, San Francisco. As a postdoc in Chris Doe’s lab at the University of Oregon, she discovered that the 3-D organization of the neural progenitor genome changes during development, determining which genes can be activated, and thus, which cell types can be generated. Now at Columbia, Kohwi is excited to embark on a journey into nuclear architecture and stem cell competence to ask fundamental questions about the origin of neural diversity during brain development.

The brain’s complexity is apparent from the incredible diversity of its neural cell types. To form the functional circuitry governing our cognitive and motor functions, neural progenitors must make each cell type at the right place, time and abundance. In both insects and mammals, stem/progenitor cells typically produce different cell types in a stereotyped order, and over the course of development they lose the ability to make the earlier-born cell types. Such “loss of competence” is a prominent feature of neural progenitors, although the underlying mechanisms are largely unknown. Using Drosophila, Kohwi and her colleagues discovered that neural progenitors undergo a developmentally timed reorganization of their genome that physically relocates genes within the 3-D nuclear space and affects the genes’ ability to turn on or off. They found that such gene repositioning in neural progenitors is highly regulated, and determines the progenitors’ potential to make specific cell types at each developmental stage. They aim to examine how neural progenitor nuclear architecture is regulated developmentally and how this regulation contributes to neural diversity. These results will provide new insights into brain development, neural developmental disorders and brain repair.
Yevgenia Kozorovitskiy +
Northwestern University

Yevgenia Kozorovitskiy

Yevgenia Kozorovitskiy earned B.A. and Ph.D. degrees from Princeton University, where she worked with Elizabeth Gould to study social experience-induced structural plasticity in the adult rodent and primate brain. She conducted postdoctoral research in the laboratory of Bernardo Sabatini at Harvard Medical School, where she investigated neural activity and neuromodulation in developmental wiring of basal ganglia circuits. She joined the faculty of Northwestern University in 2014. In addition to being a Rita Allen Foundation Scholar, Kozorovitskiy is the recipient of a Public Voices Fellowship and a Cornew Innovation Award from Northwestern University, a Sloan Research Fellowship and a Searle Scholar Award.

Major depressive disorder (MDD) is a tremendous mental health burden, with a lifetime incidence of more than 15 percent. A great promise for MDD treatment, especially for resistant and suicidal patients, lies in rapidly acting antidepressants. Yet the neurobiological plasticity mechanisms underlying rapid antidepressant effects remain poorly understood. Kozorovitskiy’s research group takes a multipronged approach to studying synapses and neural circuits implicated in depression and affect. First, they are evaluating whether rapidly acting antidepressant drugs and their functionally relevant metabolites directly facilitate the production of new synapses on genetically targeted neurons. Preliminary data indicate that the effects of rapidly acting antidepressants on synapses occur on a slower time scale and have a broader reach than expected, transcending the neural circuits typically implicated in depression. Second, interrogating neuromodulatory circuits implicated in regulation of affective state, they have discovered and characterized an important new direct interaction between dopamine, an amine important for reward-based learning, and oxytocin, a neuropeptide relevant to social affect, bonding and reproduction. Third, to facilitate the imaging of diffraction-limited nanoscale architecture of synapses, they have collaborated to develop a new imaging method that combines the strengths of two-photon excitation with structured illumination.
Julie Law +
Salk Institute for Biological Studies

Julie Law

Julie Law received a B.S. in biochemistry and biophysics from Oregon State University, where she conducted research in the laboratory of Walter Ream. She earned a Ph.D. in biochemistry at Johns Hopkins University School of Medicine, where she worked with Barbara Sollner-Webb. Following a postdoctoral fellowship with Steven Jacobsen at the University of California, Los Angeles, Law joined the faculty of the Salk Institute in 2012. In addition to being a Rita Allen Foundation Scholar, she is a recipient of a Ruth L. Kirschstein National Research Service Award from the National Institutes of Health and an L&L Nippert Charitable Foundation grant. In 2015 she was named a Hearst Foundation Development Chair at Salk.

Understanding how cells maintain genome stability is a fundamental biological question of relevance to reproductive health; numerous human diseases, including cancer; and crop yields. While it is known that modifications to chromatin (either in the form of nucleosome remodeling or the addition of chemical modifications to DNA and/or histones) play critical roles in maintaining genome stability, how they accomplish this feat remains unclear. Since mutations affecting chromatin structure in mammals are often lethal, answering such mechanistic questions requires a comparable, but more robust system, such as the plant model Arabidopsis thaliana. Indeed, the best characterized connection between chromatin and genome stability is a phenomenon first characterized in plants, wherein DNA methylation prevents the perilous movement of transposons within the genome by silencing their expression. The Law lab has described a family of Arabidopsis chromatin remodeling factors, CLSY1-4, that affect small RNA biogenesis, DNA methylation-mediated transposon silencing and DNA repair—revealing new links between several pathways critical for genome stability. Given the dual roles of the CLSY proteins, they propose to utilize these factors to dissect the connections between chromatin and genome stability. Such studies will shed light not only how DNA damage is normally repaired, but also on how chromatin-based defects cause genome instability.
John Schoggins +
The University of Texas Southwestern Medical Center

John Schoggins

RELATED STORY: Rita Allen Foundation Scholar Examines Zika Virus Infection of Brain Cells

John Schoggins (Milton E. Cassel Scholar) earned his B.S. in chemistry from the University of Rochester and his Ph.D. in molecular biology from the Weill Cornell Graduate School of Medical Sciences. He was a postdoctoral fellow in virology/infectious disease at The Rockefeller University, and has been on the faculty at UT Southwestern Medical Center in Dallas since 2012. In addition to being a Rita Allen Foundation Milton E. Cassel Scholar, he has been named a Nancy Cain and Jeffrey A. Marcus Scholar in Medical Research, in Honor of Dr. Bill S. Vowell, at UT Southwestern Medical Center and a Clayton Foundation Scholar. He has also received the Ruth L. Kirschstein National Research Service Award from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases, the NIH New Innovator Award, and both the Sidney and Joan Pestka Award for Excellence in Interferon Research and the Seymour and Vivian Milstein Young Investigator Award from the International Cytokine and Interferon Society.

Interferons are among the first lines of defense against viral infection. The interferon-induced antiviral state is established by the transcription of hundreds of interferon-stimulated genes, many of which have direct antiviral effector functions. Previous screening efforts in Schoggins’ lab identified interferon alpha-inducible protein 6 (IFI6) as an inhibitor of yellow fever virus and dengue virus infection. His group has shown that IFI6 is inhibitory toward multiple flaviviruses, in some cases reducing viral titers 1,000-fold. Strikingly, this antiviral effect is highly specific, since the closely related hepatitis C virus is not inhibited. CRISPR-mediated deletion of IFI6 results in a strong attenuation of interferon sensitivity, suggesting that IFI6 plays a major role in the antiviral response during flavivirus infections. Using a variety of molecular virological and cell biological approaches, Schoggins’ team has shown that the mechanism of IFI6 action is inhibition of viral genome replication, but not earlier steps in the viral life cycle. They are currently addressing a potential role for flavivirus NS1 protein as a target of IFI6 action. In preliminary studies, ectopic expression of NS1 was able to rescue viral infection from the inhibitory effects of IFI6. These findings uncover a novel interferon-stimulated gene that potently and selectively inhibits replication of several important disease-causing flaviviruses.
Robert Sorge +
The University of Alabama at Birmingham

Robert Sorge

Robert Sorge (Award in Pain Recipient) earned his Honors B.Sc. in psychology from McMaster University in Hamilton, Ontario, his M.A. in experimental psychology from Wilfrid Laurier University in Waterloo, Ontario, and his Ph.D. in psychology from Concordia University in Montreal, Quebec. He was a postdoctoral fellow at McGill University before joining the faculty at The University of Alabama at Birmingham in 2012. In addition to being named a Rita Allen Foundation Pain Scholar, he has received a Young Investigator Award from the Sex, Gender and Pain Special Interest Group of the International Association for the Study of Pain. He also has received postdoctoral fellowships from the Alan Edwards Center for Research on Pain at McGill and from the National Sciences and Engineering Research Council of Canada.

Obesity in America is reaching epidemic proportions, with more than one-third of the population classified as obese, and even more as overweight. In addition to the increased risk for metabolic syndromes and cardiovascular disease, obesity is also comorbid with chronic pain for a significant number of patients. It is known that adipose tissue and components of the American diet can contribute to a chronic proinflammatory state that may predispose individuals to significant negative health effects. Sorge and his collaborators believe that this state is the result of heightened activity of the immune system. Their previous work has shown that consumption of a Western diet results in changes in acute sensitivity to stimuli, increased systemic inflammation and prolonged recovery from injury. These effects are believed to be the result of chronic immune cell activation in the peripheral and central nervous system. Current work is underway to investigate the temporal profile of immune cell activation following differential exposure to the American diet in rodents. Through examination of the immune-related impact of diet, it may be possible to formulate treatments that will reduce the negative effects of the American diet with respect to pain and other related inflammatory conditions.
Jeremy Wilusz +
Baylor College of Medicine (Perelman School of Medicine at the University of Pennsylvania)

Jeremy Wilusz

Jeremy Wilusz received his Ph.D. from the Watson School of Biological Sciences at Cold Spring Harbor Laboratory and performed postdoctoral studies at the Massachusetts Institute of Technology. His research addresses the mechanisms by which noncoding RNAs are generated, regulated and function. Wilusz has been the recipient of the RNA Society/Scaringe Young Scientist Award, the Leukemia & Lymphoma Society Postdoctoral Fellowship and the National Institutes of Health Pathway to Independence Award.

It was long assumed that eukaryotic precursor mRNAs (pre-mRNAs) are almost always spliced to generate a linear mRNA that is then translated to produce a protein. However, recent deep sequencing studies have revealed thousands of protein-coding genes that are non-canonically spliced to produce circular RNAs with covalently linked ends. Some RNA circles are expressed at much higher levels than their associated linear mRNAs, suggesting that the main function of some genes may be to produce circular noncoding RNAs, not proteins. Wilusz’s research aims to reveal (i) how the choice between linear versus circular RNA production is made, (ii) how circular RNAs function and (iii) how misregulation of circular RNAs contributes to human cancer. As part of these efforts, his team has shown that circular RNA biogenesis is often initiated when complementary sequences from two different introns base-pair to one another. This brings the splice sites from the intervening exon(s) into close proximity to facilitate the backsplicing event that generates the circular RNA.They have used this knowledge to make plasmids that efficiently circularize exons in vivo, allowing them to begin to identify novel roles for circular RNAs in normal and cancer cells.
Yi Ye +
New York University

Yi Ye

Yi Ye (Award in Pain Recipient) holds a Ph.D. in neuroscience from the University of Wyoming, a master’s degree in clinical research from New York University and an M.B.A. from NYU’s Stern School of Business. She was a research fellow in the Department of Oral and Maxillofacial Surgery in the College of Dentistry at the University of California, San Francisco, and joined the Bluestone Center as an associate research scientist in 2010. She has been in her current position since 2015. She has received a Travel Award and a Young Investigator Award from the International Association for the Study of Pain, and was awarded both a National Institutes of Health-NYU-Clinical and Translational Science Institute Scholarship and an NYU Whitehead Fellowship in 2015.

Ye’s research aims to understand the neurobiological basis of cancer pain, with additional focus on carcinogenesis and tumor progression in head and neck cancer. The ultimate goal of her research is to develop novel therapies that can be used for both cancer and pain treatment by targeting shared mechanisms. In progression toward this goal, she directs a translational research program that uses multiple approaches including in vitro cell culture, animal models and human studies.

2014

Lei Ding +
Columbia University

Lei Ding

Lei Ding completed his undergraduate studies at Peking University, and earned a Ph.D. at the University of Colorado, Boulder, where he worked with Min Han. He was a postdoctoral fellow in Sean Morrison’s laboratory at the University of Michigan and The University of Texas Southwestern Medical Center. He joined the faculty of Columbia University in 2013.

A lifelong supply of blood and immune cells depends on self-renewing hematopoietic stem cells (HSCs). How HSCs self-renew is a fundamental question with broad implications for understanding development, regeneration, cancer and aging of the blood system. HSC self-renewal is regulated by cell-intrinsic and -extrinsic mechanisms. The Ding laboratory is interested in these mechanisms, particularly extrinsic mechanisms that regulate blood-forming HSC self-renewal and maintenance. Prior work has identified bone marrow perivascular mesenchymal stromal cells as a critical component of the niche.

Ding’s group is studying the extrinsic regulation of HSCs in three distinct, yet closely related, areas: 1) regulation of bone marrow perivascular mesenchymal stromal cells; 2) the cellular component of the fetal liver HSC niche; and 3) the contribution of the niche to the pathogenesis of hematological diseases. They are in the process of characterizing several candidate factors that may regulate the fate of bone marrow perivascular stromal cells. They are also elucidating the roles of several candidate niche cell types in fetal livers. In addition, their data suggest that bone marrow mesenchymal stromal cells are critical contributors to a hematopoietic malignancy, myelofibrosis, providing a cellular target to better treat the disease. HSC-based bone marrow transplantation is widely used in clinics to treat hematological diseases. Ding and his team hope to apply their knowledge to better harness the power of HSCs.
Molly Hammell +
Cold Spring Harbor Laboratory

Molly Hammell

Molly Hammell (Milton E. Cassel Scholar) holds a B.S. in physics from the College of William and Mary and a Ph.D. in physics and astronomy from Dartmouth College. The Hammell lab specializes in developing novel computational algorithms for the analysis and integration of high-throughput genomics datasets and applying these to questions of human disease. Hammell has a broad background in small RNA biology and gene regulatory network analysis, transposon biology and genomics, as well as extensive experience in the statistical analysis of next-generation sequencing data. As a postdoctoral fellow working with Victor Ambros at Dartmouth Medical School and the University of Massachusetts Medical School, she developed new algorithms to identify the targets and pathways regulated by microRNAs in animals and to profile the dynamics of small RNA activity across development. Her lab at Cold Spring Harbor Laboratory has expanded on these efforts to map the role of both microRNAs and transposon-targeting piRNAs and siRNAs in animals. This includes efforts to establish the molecular mechanisms by which transposons are controlled in somatic tissues. This also includes a major project to profile the genomes and transcriptomes of amyotrophic lateral sclerosis (ALS) patient samples in order to understand the extent to which transposons contribute to neurodegenerative disease in patients.

Our genomes are filled with viral-like sequences called transposons, many of which are capable of creating new copies of themselves that can reintegrate elsewhere in the genome, altering the function of nearby genes. While most transposon sequences are now-defunct remnants of ancient genomic parasites, a small fraction of these are still capable of activating themselves, creating genomic instability and crippling cellular function. The Hammell lab and others have discovered a link between the activity of these transposon sequences and neurodegenerative diseases related to misfunction of the RNA binding protein TDP-43 (ALS and frontotemporal lobar degeneration). However, much remains unknown about how transposons are controlled in somatic tissues such as the brain, and the extent to which their activity contributes to neurodegenerative disease. Hammell’s group is working to elucidate the connections between transposon activity and TDP-43 related diseases.
Sebastian Klinge
The Rockefeller University
Zachary Knight
University of California, San Francisco
Gregory Scherrer +
University of North Carolina at Chapel Hill School of Medicine (Stanford University School of Medicine)

Gregory Scherrer

Gregory Scherrer (Award in Pain Recipient) earned his Ph.D. in cellular and molecular biology from the University of Strasbourg, France. He completed postdoctoral training at the University of California, San Francisco, and at Columbia University. He joined the faculty at the Stanford University School of Medicine in 2012. In addition to a Rita Allen Foundation Scholar award, he has received an International Association for the Study of Pain Postdoctoral Fellowship, National Institutes of Health/National Institute on Drug Abuse K99R00 Pathway to Independence and R01 Awards, a Department of Defense Neurosensory Research Award, and an International Narcotics Research Conference Young Investigator Award, and most recently was named a New York Stem Cell Foundation – Robertson Neuroscience Investigator.

The members of the Scherrer Laboratory investigate how the nervous system generates the sensory and affective dimensions of pain experience and opioid analgesia to discover novel analgesic therapies. They aim to identify the pathological changes that occur within neural circuits when chronic pain develops, at the neural network, cellular and molecular levels. One of their approaches is to gain understanding of how our endogenous opioid system modulates pain thresholds. Opioid receptors mediate the effects of opioid painkillers, such as morphine. By determining how opioids generate analgesia and detrimental side effects (e.g., tolerance, addiction, respiratory depression), Scherrer and his team hope to develop more efficient and safer analgesics for the treatment of chronic pain. These studies will also identify novel approaches to counteract opioid side effects and battle the current opioid epidemic. To reach these goals, Scherrer’s research combines a variety of experimental approaches, including molecular and cellular biology, neuroanatomy, electrophysiology, opto- and pharmacogenetics, in vivo calcium imaging and behavior.
Lin Tian +
University of California, Davis, School of Medicine

Lin Tian

Lin Tian holds a B.S. in neuroscience from the University of Science and Technology of
China and a Ph.D. in biochemistry, molecular and cell biology from Northwestern University. She completed postdoctoral training at the Howard Hughes Medical Institute’s Janelia Farm Research Campus, where she developed a toolbox of ultrasensitive neural activity sensors that have been widely utilized. Her current work is a combination of neural activity sensor development and applications. Tian has received the National Institutes of Health Director’s New Innovator Award, Human Frontier Science Program Young Investigator Grant, Hartwell Foundation Individual Biomedical Research Award and NIH BRAIN Initiative grants.

The altered dynamics of synaptic transmission have been implicated in a number of human neurological and psychiatric diseases, including Parkinson’s, schizophrenia and addiction. However, how complex patterns of neural activity at multiple synapses interact to drive changes in circuit connectivity remains poorly defined. To address this question, we must determine the spatiotemporal relationships of different types of neurotransmitters and neuromodulators with synaptic resolution in a defined circuitry. Recent breakthroughs in modern microscopy and protein-based fluorescence sensors hold great promise to access synaptic transmission with needed molecular and cell type specificity and spatiotemporal resolutions. Tian and her collaborators have generated a sensor for the excitatory neurotransmitter glutamate and demonstrated its utility for detection of fast signaling events in worm, fish, fly and mouse. To further expand the kinds of neural activity that can be measured with genetically encoded indicators, they applied the established sensor design and optimization platform to the development of a set of specific, targetable and sensitive sensors for direct measurement of neurotransmitters, including gamma-aminobutyric acid and the biogenic amines. Application of these imaging tools will enable neuroscientists to obtain a dynamic and comprehensive view of synaptic transmission in action to decipher the codes for transferring information across neural circuitry and systems.
Tuan Trang +
University of Calgary

Tuan Trang

RELATED STORY: Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Tuan Trang (Award in Pain Recipient) began his research career as an undergraduate at Queen’s University studying the effects of prenatal alcohol exposure. He also completed a Ph.D. in pharmacology and toxicology there, researching the spinal mechanisms of opioid analgesia with the goal of developing new pharmacological strategies for improving pain therapy. He pursued postdoctoral training as a Canadian Institutes of Health Research (CIHR) fellow in the laboratory of Dr. Michael Salter at the Hospital for Sick Children in Toronto. He has received a CIHR New Investigator Award, and young investigator awards from the Canadian Association for Neuroscience and Canadian Society for Pharmacology and Therapeutics. His research has been supported by grants from, in addition to the Rita Allen Foundation, the CIHR, the Natural Sciences and Engineering Research Council of Canada, a Vi Riddell Pain Grant from the University of Calgary and the Canada Foundation for Innovation.

Opioids are among the most powerful and widely prescribed drugs for treating pain. However, a major problem in terminating opioid pain therapy is the debilitating withdrawal syndrome that can plague chronic opioid users. The mechanisms involved in opioid withdrawal are poorly understood, and the limited clinical strategies for treating withdrawal are ineffective. Trang and his collaborators have identified the pannexin-1 (Panx1) channel as a novel therapeutic target for treating morphine withdrawal. They discovered that morphine treatment induces synaptic plasticity in spinal lamina I/II neurons, which manifests as long-term synaptic facilitation upon naloxone-precipitated morphine withdrawal. This synaptic facilitation is critically gated by activation of Panx1 channels expressed on microglia. Pharmacologically blocking Panx1, or genetically ablating this channel specifically from microglia, blocked spinal synaptic facilitation and alleviated the behavioral sequelae of morphine withdrawal. Their findings together reveal a novel mechanism by which microglia signal through Panx1 to produce the cellular and behavioral corollary of withdrawal. Thus, targeting Panx1 represents a potential novel therapeutic approach for treating the symptoms of opioid withdrawal. Trang and his team are moving these discoveries into the clinic by building on the utility of probenecid as a unique and practical therapy for the management of opioid withdrawal. In a pilot clinical trial, they will test whether probenecid alleviates opioid withdrawal in patients undergoing opioid tapering, a systematic and gradual approach intended to reduce or discontinue opioid use.

2013

Michael Boyce +
Duke University School of Medicine

Michael Boyce

Michael Boyce obtained his B.A. in biochemistry from Harvard College and his Ph.D. in cell biology from Harvard Medical School in the laboratory of Ying Yuan. He performed postdoctoral research in chemical biology and glycobiology at the University of California, Berkeley, with Carolyn Bertozzi, and has been an Assistant Professor of Biochemistry at the Duke University School of Medicine since 2012. Boyce has received fellowships or career awards from the Albert J. Ryan Foundation, the National Science Foundation, the Life Sciences Research Foundation/Howard Hughes Medical Institute, the Whitehead Scholars Program, the Sydney Kimmel Foundation for Cancer Research and the Mizutani Foundation for Glycoscience, in addition to his 2013 Rita Allen Foundation Scholar award. Boyce is also active in promoting diversity and inclusion in the biosciences and serves on the national Minorities Affairs Committee of the American Society for Cell Biology.

The long-term goal of the Boyce lab is to understand the role of protein glycosylation in mammalian cell signaling and physiology. Protein glycosylation is the most abundant post-translational modification in nature and, as a sugar-based modification it lies at the nexus of cell signaling and cell metabolism. However, because glycosylation is a dynamic, non-templated and chemically complex process, it can be difficult to study with conventional biological techniques alone. The lab uses a range of biochemical, cell, chemical and structural biology methods to dissect the role of protein glycosylation in mammalian cells. Current work focuses on two specific aspects of glycosylation: first, understanding how dynamic signaling by O-linked b-N-acetylglucosamine on intracellular proteins senses and regulates cell physiology; and second, investigating the cell- and systems-level regulation of nucleotide-sugar metabolites in health and disease.
Sophie Dumont +
University of California, San Francisco

Sophie Dumont

Sophie Dumont (Milton E. Cassel Scholar) received her B.A. in physics from Princeton University, and Ph.D. in biophysics from the University of California, Berkeley, where she probed the mechanics of individual biomolecules with Carlos Bustamante. She was a junior fellow at the Harvard Society of Fellows and a postdoc at Harvard Medical School, where she worked on the mechanics of cell division with Tim Mitchison. She has been an assistant professor at UCSF since 2012, and her group focuses on the self-organization and emergent mechanics that drive robust chromosome segregation. In addition to being a Rita Allen Foundation Scholar, she is a Searle Scholar, a Sloan Research Fellow, and a National Institutes of Health New Innovator and National Science Foundation CAREER award recipient.

Life is a chemical as well as a mechanical process. At the nanometer scale, mechanoenzymes interconvert force and chemical potential. At the micrometer scale, cells spatially organize their constituents, change shape and move. At the millimeter scale, organisms develop and also move. How are mechanical and chemical processes integrated over molecular, cellular and tissue-length scales?

The Dumont lab aims to understand how cells coordinate mechanical and chemical activities to equally distribute their genetic material when they divide. During cell division, each daughter cell must inherit exactly one copy of each chromosome. Errors can lead to cell death or cancer in somatic cells, and developmental disorders in the germ line. How do cells generate, detect and respond to mechanical force to robustly and accurately segregate their chromosomes? How do the spindle’s nanometer-scale constituents work together to generate micrometer-scale movements?

To address these questions, the Dumont lab uses an interdisciplinary approach to uncover how molecules, mechanics and cellular function relate to each other.
Dorothea Fiedler
Leibniz-Institut für Molekulare Pharmakologie (Princeton University)
Elena Gracheva +
Yale University School of Medicine

Elena Gracheva

Elena Gracheva received an M.S. in biochemistry from Moscow State University and a Ph.D. in neuroscience from the University of Illinois at Chicago, where she worked with Janet Richmond. She conducted postdoctoral research at the University of California, San Francisco, in the laboratory of David Julius. She joined the faculty of the Yale University School of Medicine in 2012. In addition to being a Rita Allen Foundation Scholar, Gracheva has received a Yale Scholar Award in Neuroscience, an Alfred P. Sloan Foundation research fellowship and a Beckman Foundation Young Investigator award.

The main goal of Gracheva’s lab is to understand the molecular basis of temperature sensitivity under normal, adaptive and pathological conditions. Her early work concerned acute temperature perception in infrared-sensing animals. She and her colleagues discovered two receptors that are responsible for this function, as well as structural elements within ion channels that dictate activation by temperature and chemicals. Her research group is using non-standard animal models—hibernating thirteen-lined ground squirrels and Syrian hamsters—to delineate molecular and cellular aspects of somatosensitivity, with a focus on temperature tolerance. They are investigating the contribution of different ion channels to cold tolerance of mammalian hibernators using a multidisciplinary approach, which includes electrophysiology, molecular biology, imaging, behavioral paradigms, genomics, transcriptomics and bioinformatics. Recently, Gracheva’s group discovered a molecular mechanism that supports nerve tissue function during hibernation.
William James Greenleaf +
Stanford University School of Medicine

William James Greenleaf

William Greenleaf received an A.B. in physics from Harvard University, and received a Gates Fellowship to study computer science for one year at Trinity College in Cambridge, England. After this experience abroad, he returned to Stanford to carry out his Ph.D. in applied physics in the laboratory of Steven Block, where he investigated, at the single-molecule level, the chemo-mechanics of RNA polymerase and the folding of RNA transcripts. He conducted postdoctoral work in the laboratory of Xiaoliang Sunney Xie at Harvard University, where he was awarded a Damon Runyon Cancer Research Foundation Fellowship, and developed new fluorescence-based high-throughput sequencing methodologies. Since moving to Stanford in 2011, he has been named a Baxter Foundation Scholar, as well as a Rita Allen Foundation Scholar. In addition to his position in the Department of Genetics, Greenleaf holds a courtesy appointment in Stanford’s Department Applied Physics. He is a member of Bio-X, the Biophysics Program, the Biomedical Informatics Program and the Cancer Center. He is also a participating member in a number of large genomic consortia (CEGS, GGR).

High-throughput sequencing techniques are revolutionizing biology and promise to have a significant impact on the future of medicine. Greenleaf’s research interests focus on leveraging high-throughput methods to understand “the physical genome” by developing methods to probe both 1) the relationship between DNA sequence and the structure and function of molecules encoded by the genome; as well as 2) the physical compaction and folding of the genome itself, and how this topology influences biological state. 1) His research group is interested in understanding the biophysical basis and evolutionary consequences of sequence-function relationships in biological molecules and their interactions. Toward this goal, they develop ultra-high-throughput methods to quantitatively assay sequence-space in bulk and single-molecule experiments. 2) They also seek to understand the hierarchical folding of genomic DNA into regulated structures, the most basic and important of which is the nucleosome. With this objective in mind, they have developed methods that assay open chromatin, nucleosome positions and transcription factor binding genome-wide in small populations of cells undergoing dynamic processes such as differentiation or stochastic state switching.
Rebecca Seal +
University of Pittsburgh

Rebecca Seal

RELATED STORY: Rita Allen Foundation Scholars Advance Understanding of Nervous Systems in Health and Disease

Rebecca Seal (Award in Pain Recipient) earned her B.S. in chemistry and psychology from the University of Oregon and her Ph.D. in neuroscience from Oregon Health and Science University. Her graduate studies with Susan Amara focused on the structure and function of plasma membrane glutamate transporters. As a postdoctoral scholar at the University of California, San Francisco, she studied the vesicular glutamate transporter 3 in hearing and pain with Robert Edwards. She has received a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation, an Innovation Award from the American Diabetes Association, a Japanese Society for the Promotion of Science Fellowship and a Whitehall Foundation Research Award.

Seal’s laboratory focuses on defining the neural circuitry underlying a wide range of nervous system functions in health and disease, including persistent pain, motor symptoms of Parkinson’s disease and audition. A major impediment to identifying new pain treatments is incomplete understanding of the neural networks and mechanisms that underlie the pain. Her team’s work, using multiple approaches ranging from cellular and molecular to physiological and behavioral, centers on elucidating the neural circuits and mechanisms that underlie a particular form of persistent pain in which touch becomes painful in the setting of injury, termed mechanical allodynia. The spinal cord dorsal horn is a major site for the integration of somatosensory information and is vital for the induction and maintenance of this form of pain. Their work thus far suggests that the pain is encoded by distinct microcircuits in the dorsal horn, depending on the nature of the injury. This concept not only has important implications for understanding at a basic level how the nervous system encodes mechanical allodynia, but also highlights the need to consider etiology in the design and implementation of therapeutic strategies.
Reza Sharif-Naeini +
McGill University

Reza Sharif-Naeini

RELATED STORY: Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Reza Sharif-Naeini (Award in Pain Recipient) earned his Ph.D. in physiology from McGill University in 2007, and returned there to joined the faculty in 2012. In the interim, he was a postdoctoral fellow at Institut Pharmacologie Moleculare et Cellulaire in Nice, France, and in the Department of Anatomy at the University of California, San Francisco. He has received fellowships from the Canadian Institutes of Health Research, the International Association for the Study of Pain and the Human Frontier Science Program. He has also received the CIHR Brain Star Award for excellence in research and the Peter and Patricia Gruber International Research Award in Neuroscience from the Society for Neuroscience.

Chronic neuropathic pain (NeP) is a debilitating disease that follows nerve injury and persists long after the initial injury has subsided. Despite the plethora of medications and treatment modalities, NeP remains a disease with unmet medical needs that significantly decreases patients’ quality of life. Spontaneous pain and mechanical allodynia, two hallmarks of NeP, are due in part to a spinal cord dysfunction characterized by a decrease in inhibitory neurotransmission (or inhibitory tone). Our understanding of how these inhibitory mechanisms function in health and disease remains, however, limited. This indicates a need for novel and innovative experimental approaches to gain a better understanding of inhibitory circuits in the dorsal horn and how changes in these circuits can precipitate NeP symptoms. Sharif-Naeini’s group is interested in understanding the function of these inhibitory pathways using transgenic mouse lines combined with opto/pharmacogenetic approaches.

2012

Sreekanth Chalasani +
Salk Institute for Biological Studies

Sreekanth Chalasani

RELATED STORIES: Rita Allen Foundation Scholar Harnesses Sound Waves to Activate Brain Cells, Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Sreekanth Chalasani obtained a B.S. degree and an advanced diploma in computer science from Osmania University in Hyderabad, India. He then did research at the National Center for Biological Sciences in Bangalore, India, before coming to the U.S. in 1997. Chalasani obtained a Ph.D. from the University of Pennsylvania, where he worked with Jonathan Raper, and did postdoctoral research in Cornelia Bargmann’s laboratory at the University of California, San Francisco, and The Rockefeller University. He started his laboratory at the Salk Institute for Biological Studies in 2010. In addition to the Rita Allen Foundation award, Chalasani has received awards including a Blavatnik Award for Young Scientists, a Basil O’Connor Starter Award from the March of Dimes, and a W.M. Keck Foundation Award.

Chalasani’s research addresses how the brain responds to changes in its surrounding environment. Neural circuits within the brain extract relevant information from the environment and regulate behaviors on timescales ranging from seconds to hours. A complete understanding of this process requires an ability to identify, record and manipulate all the participating neurons. It is difficult to obtain this level of access in a complex vertebrate brain. Chalasani’s group is using the nematode C. elegans, with its small, well-defined nervous systems, to decode the cellular and molecular mechanisms transforming environmental changes into behaviors. They have shown that C. elegans can evaluate the size of a patch of bacteria (its food) and uses that information to modify a behavior that lasts many minutes. In particular, they have identified sensory neurons that encode the size of a food patch by detecting large, but not small, changes in food. Moreover, they show that information about patch size is stored in the level of dopamine in the circuit, which acts to modify downstream sensory and interneurons. Also, they find that the rate of acquiring information is controlled by the amount of CREB protein in key interneurons in the circuit.
Christopher Hammell +
Cold Spring Harbor Laboratory

Christopher Hammell

Christopher Hammell (Milton E. Cassel Scholar) attended the University of Georgia, where he received a B.S. degree in biochemistry. He then moved to Dartmouth Medical School, where he studied the mechanisms by which mRNA molecules are exported from the nucleus. After receiving his Ph.D., he began work with Victor Ambros at the University of Massachusetts, investigating how animals regulate the activity of microRNAs during development. He discovered a family of proteins, the TRIM-NHL family, that physically associate with and modulate the activity of the microRNA-induced silencing complex.

Hammell then began his independent research program at Cold Spring Harbor Laboratory, where he switched his focus toward understanding how the temporal precision of developmental events is established. His current work centers on determining the regulatory architectures that ensure that developmental genes are turned on and off at the correct times.
Michael Jankowski +
Cincinnati Children’s Hospital Medical Center

Michael Jankowski

Michael Jankowski (Award in Pain Recipient) earned an M.S. in neuroscience and a Ph.D. in neurobiology from the University of Pittsburgh, where he also conducted postdoctoral research. He joined the faculty of the Cincinnati Children’s Hospital Medical Center in 2011. Jankowski has received several National Institutes of Health grants from the National Institute of Neurological Disorders and Stroke, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Arthritis,Musculoskeletal and Skin Diseases. He also is a recipient of an International Association for the Study of Pain (IASP) Early Career Research Grant Award, and was named a Cincinnati Children’s Trustee Scholar in addition to being a Rita Allen Scholar. He serves on numerous grant review panels and journal review boards and is an associate editor for the journal PAIN and reviewing editor for Molecular Pain. He is on the training faculty in the Neuroscience Graduate Program and the Molecular and Developmental Biology Graduate Program at CCHMC. He is also a member of the Society for Neuroscience, the IASP and the American Pain Society.

Jankowski’s lab is interested in the peripheral mechanisms of pain development under unique injury conditions. His research has two main focuses: peripheral mechanisms of musculoskeletal pain, specifically in the context of ischemia; and the consequences of neonatal injury on developing sensory neurons. Ischemic muscle pain is a major health issue that occurs in numerous disorders, such as sickle cell anemia, peripheral vascular disease and even fibromyalgia. Many patients experience altered cardiovascular reflexes and musculoskeletal pain as a result of these disease states. Chronic pain in children, however, can arise from multiple sources, including surgery, inflammation or even neonatal intensive care. Yet we do not have a comprehensive understanding of the changes that occur in specific subtypes of sensory fibers after ischemic muscle injury or during postnatal development that modulate these distinctive pain states. Jankowski’s group utilizes a multidisciplinary experimental approach to obtain a broad understanding of pain development at the primary afferent level. These studies will hopefully lead to the development of treatments for adverse changes in cardiovascular reflexes or musculoskeletal pain associated with muscle ischemia, or novel therapies for pediatric pain.
Xin Liu +
The University of Texas Southwestern Medical Center

Xin Liu

Xin Liu earned an undergraduate degree in biochemistry from Nanjing University in China and a Ph.D. in chemistry from the University of Pennsylvania, where he conducted research in the laboratory of Ronen Marmorstein, carrying out structural and functional studies on the retinoblastoma and p300/CBP tumor suppressor proteins and their regulation by viral oncoproteins. Liu was a Jane Coffin Childs postdoctoral fellow in the laboratory of Roger Kornberg at Stanford University, where he studied the molecular basis of eukaryotic transcription. He is a W.W. Caruth, Jr. Scholar in Biomedical Research of the UT Southwestern Medical Center and a CPRIT Scholar in Cancer Research of the Cancer Prevention and Research Institute of Texas.

In eukaryotes such as humans, genomic DNA is wrapped around histone proteins to be packaged into chromatin fiber. The 3-D chromatin structure exerts a profound impact on gene expression and is associated with human diseases, including cancer and developmental disorders, when dysregulated. Liu’s research is focused on understanding the structural and biophysical basis for formation of chromatin loop and facultative heterochromatin mediated by large macromolecular assemblies. His laboratory mainly uses X-ray crystallography, cryo-electron microscopy, biochemical reconstitution and deep sequencing to achieve its research goals.
Michael Long +
New York University School of Medicine

Michael Long

RELATED STORY: Rita Allen Foundation Scholar Michael Long Reveals How Brain Circuits Help Birds Learn to Sing

Michael Long received a B.S. in biology and a B.A. in psychology from Rhodes College, and earned a Ph.D. in neuroscience from Brown University, where he worked with Barry Connors. He conducted postdoctoral research in the laboratory of Michale Fee at the Massachusetts Institute of Technology, and joined the faculty of the New York University School of Medicine in 2010. In addition to being a Rita Allen Foundation Scholar, Long has received an Esther A. and Joseph Klingenstein Fellowship Award in the Neurosciences and a Robertson Neuroscience Investigator award from the New York Stem Cell Foundation.

Sequential activity appears to be a broad feature in neural circuits and is thought to play an important role in orchestrating complex behaviors. These sequences can be generated in a number of ways, although we know very little about their underlying connectivity, making it difficult to predict a precise mechanism. Long and his colleagues have taken an anatomical approach to understand connectivity in the zebra finch HVC, a premotor circuit that drives a complex learned vocal sequence. Previous work suggested that the neural sequence in HVC emerges from a chain of synaptically connected projection neurons, but anatomical evidence for such direct synaptic connections is lacking. Long’s group identified a large number of premotor-premotor contacts and characterized their distribution along the dendrites and axon collaterals. Surprisingly, they found that proximal and distal connectivity is highly cell-type specific. Locally, premotor neuron axons primarily target interneurons, while distally they form most of their synapses with excitatory neurons, many of which are onto other premotor neurons. Their results show that monosynaptically connected premotor neurons are spatially decorrelated and suggest that the chain is propagated through linked winner-take-all modules.
Luciano Marraffini +
The Rockefeller University

Luciano Marraffini

RELATED STORIES: Foundation Scholars Earn NIH Awards for High-Risk, High-Reward Research, Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change
Sarah Ross +
University of Pittsburgh

Sarah Ross

Sarah Ross (Award in Pain Recipient) earned her B.Sc. from the University of Western Ontario and her Ph.D. from the University of Michigan, both in physiology. She was a postdoctoral fellow in the Department of Neurobiology at Harvard Medical School, where she worked with Michael Greenberg. She joined the faculty at the University of Pittsburgh in 2011. In addition to the Rita Allen Foundation, she has received support for her work from the National Institutes of Health.

The spinal cord plays a critical role in processing somatosensory information. To study these spinal microcircuits, the Ross lab has developed a novel somatosensory preparation that allows recording from the output neurons (via retrograde labeling of spinal projection neurons) while controlling somatosensory input (via natural stimulation of the skin) and simultaneously manipulating activity of specific populations of spinal interneurons (via the combination of Cre alleles and optogenetics). Using this physiological preparation, the Ross lab is addressing long-standing questions in the field of somatosensation, such as: How is itch distinguished from pain? Why does scratching relieve itch? and How does pain become abnormally amplified upon injury?

2011

Briana Burton +
University of Wisconsin-Madison (Harvard University)

Briana Burton

RELATED STORY: Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Briana Burton (Milton E. Cassel Scholar) earned a B.A. from Northwestern University and a Ph.D. from the Massachusetts Institute of Technology. She was a faculty member in the Department of Molecular and Cellular Biology at Harvard University from 2008 to 2015, when she became an assistant professor at the University of Wisconsin-Madison. Burton received postdoctoral fellowship awards from the Damon Runyon Cancer Research Foundation and the Charles A. King Trust. She has been honored with the William F. Milton Award and the Fannie Cox Prize for Excellence in Science Teaching. From 2010 to 2011 she was an education fellow of the National Academy of Sciences. She is currently a Distinguished Lecturer of the American Society for Microbiology.

Every day in the laboratory, scientists take for granted the immensely powerful process of transformation, whereby cells bind, internalize and incorporate exogenous DNA. In many cases, whether for research or therapeutic purposes, a major limitation to progress is the ability to genetically manipulate cells. How exactly do cells move one of the largest and most hydrophilic biological molecules across hydrophobic membrane barriers? Whereas we tend to think of DNA uptake in terms of the artificial processes imposed by researchers on their cells, nature has dedicated protein machinery for binding and internalizing DNA. In fact, the majority of the bacterial species sequenced to date appear to code for such DNA uptake machines.

The long-term goal of the Burton laboratory is to understand natural mechanisms cells use to transport DNA across cell membranes. They use the naturally transformable model bacterium Bacillus subtilis and a combination of biochemistry, classical microbiology and high-resolution imaging for the molecular characterization of the most mysterious part of bacterial transformation, the core protein apparatus that allows DNA entry to the cell.
Elissa Hallem +
University of California, Los Angeles

Elissa Hallem

RELATED STORY: Rita Allen Foundation Scholars Advance Understanding of Nervous Systems in Health and Disease

Elissa Hallem received her B.A. in biology and chemistry from Williams College and her Ph.D. in neuroscience from Yale University, where she studied the role of odorant receptors in odor coding in the laboratory of John Carlson. She conducted postdoctoral research with Paul Sternberg at the California Institute of Technology. Hallem joined the faculty of UCLA in 2011, and in 2012 she was selected as a MacArthur Fellow. She has also received a John H. Walsh Young Investigator Research Prize from the David Geffen School of Medicine, a Burroughs-Wellcome Fund Investigators in the Pathogenesis of Disease Award, a National Institutes of Health Director’s New Innovator Award (DP2), a McKnight Scholar Award, a UCLA Dean’s Recognition Award, a Searle Scholar Award and an Alfred P. Sloan Research Fellowship.

The Hallem laboratory is studying the neural basis of parasitic behaviors using the host-seeking behaviors of skin-penetrating parasitic nematodes as a model system. Skin-penetrating nematodes infect approximately 1 billion people worldwide, and are responsible for some of the most common neglected tropical diseases. The infective larvae of skin-penetrating nematodes search for hosts to infect using host-emitted sensory cues, yet their host-seeking behaviors are poorly understood. Hallem’s group is conducting an in-depth analysis of host seeking in the skin-penetrating human threadworm Strongyloides stercoralis. They are focusing on the responses of these parasites to human skin and sweat odorants, carbon dioxide and heat. They are comparing the sensory behaviors of S. stercoralis to those of other parasitic nematodes to gain insight into how sensory behaviors differ in species with different host ranges and infection modes. They are also investigating the neural basis of host-seeking behavior. Their studies of the neural microcircuits that mediate host seeking will provide insight into how parasite sensory systems support parasite-specific behavioral repertoires, and may enable the development of new strategies for combating harmful nematode infections.
Rahul Kohli +
Perelman School of Medicine at the University of Pennsylvania

Rahul Kohli

RELATED STORY: Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Rahul Kohli obtained a B.S. in biochemistry from the University of Michigan and an M.D. from Harvard Medical School, where he also conducted Ph.D. studies under Christopher T. Walsh. He subsequently completed clinical training in internal medicine and infectious diseases and conducted postdoctoral studies with James Stivers at Johns Hopkins University. In 2010 Kohli joined the faculty of the University of Pennsylvania. His research has garnered support from the Doris Duke Foundation and the Burroughs Wellcome Fund, as well as a National Institutes of Health Director’s New Innovator Award. Kohli’s studies on the role of cytosine-modifying enzymes in adaptive immunity and pluripotency have been supported by awards from the NIH and the Rita Allen Foundation.

Since the decoding of the human genome, it is increasingly evident that nature’s diversity is not fully explained by the simple, static sequence of DNA. The genome constantly undergoes transformation through chemical modification of DNA bases, which adds an additional and essential layer of complexity. While these chemical transformations can be purposeful, yielding variety in cell lineages or in antibody molecules, they can also pose significant risks. Most notably, aberrant action of these DNA-modifying pathways can promote oncogenesis. Many of these significant modifications are focused on cytosine residues throughout the genome, with alterations that include methylation, deamination or oxidation. Understanding the enzymes and pathways that catalyze the modification of cytosine can provide insight into how purposeful alterations are promoted over oncogenic transformations. Kohli’s research has helped to reveal the previously enigmatic mechanism by which cytosine bases can be demethylated—a transformation that is critical to the generation of pluripotent stem cells, but one that can also promote myeloid cancers when perturbed. His group’s work has revealed a nonessential role for AID/APOBEC family enzymes in demethylation and helped to establish an oxidation-repair mediated pathway for demethylation initiated by TET family enzymes.
Michael Lin +
Stanford University School of Medicine

Michael Lin

RELATED STORY: Rita Allen Foundation Scholars Advance Understanding of Nervous Systems in Health and Disease

Michael Lin received a bachelor’s degree in biochemistry from Harvard University and a Ph.D. in neuroscience from Harvard Medical School, where he worked with Michael Greenberg. He completed his medical training at the University of California, Los Angeles, and conducted postdoctoral research in Roger Tsien’s laboratory at the University of California, San Diego. In 2009 Lin joined the faculty of the Stanford University School of Medicine. In addition to a Rita Allen Foundation award, he has received a Pioneer Award from the National Institutes of Health, a Burroughs Wellcome Fund Career Award for Medical Scientists, and a Jane Coffin Childs Memorial Fund for Medical Research Fellowship.

Lin’s research group specializes in applying structure-based protein engineering to invent new molecular tools for optical reporting and optical control of neuronal and synaptic functions. The tools they develop respond over various timescales, spanning from milliseconds to days. Tools they have invented by modifying and combining protein domains in novel ways include: (1) optical voltage indicators that are uniquely fast, responsive and two-photon-compatible; (2) optical reporters that enhance deep-tissue imaging; (3) the only completely genetically encoded method for optical control of protein interactions; (4) a general architecture for single-chain optically controllable proteins; (5) optical reporters of newly synthesized proteins; and (6) chemical controllers of new protein synthesis.

In addition to inventing molecular tools, Lin’s team has been applying these tools to previously intractable neurobiological problems. Using optical reporters of protein synthesis, they have found that the synaptic structural protein PSD95 is newly synthesized and expressed at activated synapses, and that this effect is abolished in a mouse model of Fragile X mental retardation. Interestingly, the loss of new PSD95 in the Fragile X model can be rescued by partial inhibition of the TOR pathway, implying that TOR pathway regulation may be one therapeutic approach to Fragile X syndrome.
Axel Nimmerjahn +
Salk Institute for Biological Studies

Axel Nimmerjahn

RELATED STORY: Rita Allen Foundation Scholars Advance Understanding of Nervous Systems in Health and Disease

Axel Nimmerjahn completed his Boehringer Ingelheim Fonds-supported Ph.D. in physics in the laboratories of Fritjof Helmchen and Bert Sakmann at the Max Planck Institute for Medical Research/University of Heidelberg, Germany. Following his Alexander von Humboldt and Human Frontier Science Program-supported postdoctoral training with Mark Schnitzer and Ben Barres at Stanford University, he joined the Salk Institute for Biological Studies in the Waitt Advanced Biophotonics Center. Nimmerjahn’s work has been recognized by a variety of awards, including the Du Bois-Reymond Award of the German Physiologic Society, the Otto Hahn Medal and Award of the Max Planck Society, and the DP2/New Innovator and EUREKA Awards of the National Institutes of Health.

The human central nervous system (CNS) consists of an incredibly diverse set of cells, and each cell type carries out highly specialized functions in cellular networks of dazzling complexity. While much research has focused on understanding the circuits formed by neurons, brain cells called glia are equally pervasive and account for roughly an equal number of cells in the human CNS. Glial cells were long believed to play a merely passive, supportive role. However, it is becoming increasingly clear that glia make crucial contributions to CNS formation, operation and adaptation. Additionally, glial cells are involved in practically all CNS injuries and diseases. This makes glia promising targets for future therapeutic interventions. Nimmerjahn’s lab has spearheaded the development of new microscopy techniques to visualize the dynamics of glial cells and their functional cellular interactions in the living CNS. His team has worked to shrink the size of microscopes to make them wearable, allowing them to reveal how cellular activity relates to animal behavior. They have created new tools for cell type-specific staining and genetic manipulation and for analysis of large-scale imaging data. This has allowed them to address long-standing questions regarding the role of glia in the intact healthy and diseased CNS.
E. Alfonso Romero-Sandoval +
Wake Forest School of Medicine (Presbyterian College School of Pharmacy, Dartmouth Medical School)

E. Alfonso Romero-Sandoval

Alfonso Romero-Sandoval (Award in Pain Recipient) is originally from Guatemala, and received his M.D. degree from Universidad de San Carlos de Guatemala in 1999 and his Ph.D. degree in neuroscience from Universidad de Alcalá de Henares, Spain, in 2003. He did postdoctoral training at Wake Forest University and at Geisel Dartmouth Medical School. He has served on the faculty at Geisel Dartmouth Medical School and Presbyterian College School of Pharmacy. Romero-Sandoval is currently associate professor of anesthesiology at Wake Forest School of Medicine and is studying the molecular mechanisms of macrophages and their role in wound healing and in the transition from acute to chronic pain, and the use of nanotechnology to promote surgical wound healing and to prevent the development of chronic postoperative pain. Other projects include the role of cannabinoid receptor activation in skin cells for induction of analgesia, the role of endocannabinoids in postoperative pain, and the function of phosphatases and kinases in the spinal cord and periphery in the context of pain.

Romero-Sandoval’s lab uses a clinically relevant cell target gene therapy method using nanotechnology (successfully used in HIV-positive patients for gene induction) for human macrophages. The final goal of this project is to target macrophages to induce a cellular phenotype that drives the efficient resolution of inflammation and prevents the development of chronic pain following major surgeries. His team uses nanoparticles to specifically target macrophages. Romero-Sandoval proposes to induce specific genes that are involved in the resolution of inflammation by driving an M2 macrophage phenotype.
Yuan-Xiang Tao +
Rutgers New Jersey Medical School (Johns Hopkins University School of Medicine)

Yuan-Xiang Tao

Yuan-Xiang Tao (Award in Pain Recipient) earned B.Sc., M.Sc. and M.D. degrees from Nanjing Medical University, and holds a Ph.D. in neuroscience from the Shanghai Brain Research Institute of the Chinese Academy of Sciences. He completed a postdoctoral fellowship at the University of Virginia Health Sciences Center, where he studied the role of postsynaptic density proteins in chronic pain and anesthesia. Tao was a faculty member in the Department of Anesthesiology and Critical Care Medicine at Johns Hopkins University School of Medicine from 1999 to 2013, when he became a full professor at Rutgers New Jersey Medical School. Tao has received funding from the National Institutes of Health, the National Natural Science Foundation of China, the Blaustein Pain Research Fund, the David H. Koch Prostate Cancer Research Fund and the Brain Science Institute of Johns Hopkins Medicine. In 2017 he was selected for Rutgers New Jersey Medical School’s Faculty of the Year Award, as well as an Excellence in Research Award from the New Jersey Health Foundation.

Tao’s research focuses on understanding the molecular and cellular mechanisms that underlie chronic pain and opioid-induced analgesic tolerance and hyperalgesia. Research projects in his laboratory have attempted to address questions regarding different aspects of pain and opioid analgesia: 1) how protein translation is regulated under the conditions of chronic opioid tolerance and hyperalgesia; 2) how epigenetic modifications participate in the development and maintenance of chronic pain; and 3) how acute vaso-occlusive episodes induce and aggravate sickle cell disease-associated pain.

2010

Seena Ajit +
Drexel University

Seena Ajit

Seena Ajit (Award in Pain Recipient) received her Ph.D. in molecular biology from Rutgers University, and was a scientist in Neuroscience Discovery at Wyeth Research from 2001 to 2009, when she became an assistant professor at Drexel University College of Medicine.

Epigenetics is now recognized as an important aspect of gene regulation, and epigenetic analysis is likely to play an increasingly important role in the diagnosis, prognosis and treatment of diseases. Ajit is interested in pursuing various aspects of epigenetics, including DNA methylation, histone modifications and RNA-mediated gene silencing, all aimed at understanding the molecular mechanisms underlying pain. Currently her group is studying the role of noncoding RNAs in mediating pain, as well as their utility for biomarkers. They have identified differentially expressed circulating miRNAs in whole blood from patients with complex regional pain syndrome relative to controls. Additionally, studies using blood samples from good and poor responders to ketamine treatment have identified differential miRNA signatures both before and after therapy. A major focus in the lab now is to understand the significance of miRNA alterations in regulating gene expression leading to inflammation and pain.

Circulating miRNAs in bodily fluids are delivered to recipient cells via exosomes. Intercellular communication once thought to be limited to secreted signals can now be attributed to exosomes. Exosome contents, including miRNAs and mRNAs, are capable of modulating gene expression in the recipient cells. Ajit’s lab is investigating the mechanistic basis of pro- and anti-nociceptive roles of exosomes from various sources, including patients and rodent models of pain.
Diana Bautista +
University of California, Berkeley

Diana Bautista

RELATED STORY: Diana Bautista: An Itch for Knowledge

Diana Bautista (Award in Pain Recipient) earned her B.S. in biology from the University of Oregon and her Ph.D. in neuroscience from Stanford University, where she worked in the laboratory of Richard Lewis. She was a postdoctoral fellow at the University of California, San Francisco, collaborating with David Julius. She joined the Berkeley faculty in 2008. In addition to a Rita Allen Foundation Scholar award, she has received the National Institutes of Health Director’s New Innovator Award.

Bautista’s lab aims to understand the molecular mechanisms underlying the sensations of itch, touch and pain. Humans rely on these senses for a broad range of essential behaviors. For example, acute pain acts as a warning signal that alerts us to noxious mechanical, chemical and thermal stimuli, which are potentially tissue damaging. Likewise, itch sensations trigger reflexes that may protect us from disease-carrying insects. Despite these essential protective functions, itch and pain can outlast their usefulness and become chronic. Bautista’s lab uses cellular physiology, molecular biology, molecular genetics and behavioral studies to elucidate the molecular mechanisms underlying itch and pain transduction under normal and pathophysiological conditions.
Randy Bruno +
University of Oxford (Columbia University)

Randy Bruno

Randy Bruno earned his B.S. in cognitive science from Carnegie Mellon University and his Ph.D. in neurobiology from the University of Pittsburgh School of Medicine, where he worked with Daniel Simons. He was a postdoctoral fellow at the Max Planck Institute for Medical Research in Germany in the laboratory of Bert Sakmann, and joined the faculty of Columbia University in 2007. He has been a Klingenstein Fellow, a Grossman-Kavli Scholar and a Ludwig Schaefer Research Scholar, and has won the Dr. Harold and Golden Lamport Research Award in the Basic Sciences and the Society for Neuroscience Young Investigator Award.

The cerebral cortex is a key brain structure underlying cognition—all of our higher mental abilities, including sensation, perception, problem solving, decision-making and motor planning. Bruno and his colleagues recently discovered that, rather than being a monolithic structure, the cerebral cortex may contain two entirely different structures working in parallel. Signals from sensory organs are relayed to the cortex via the thalamus. Each axon from the thalamus densely targets the upper half of the cortex, while only sparsely targeting deeper cortical layers. Bruno’s team has shown that, while the axonal branches in the deep layers are relatively sparse, they still account for numerous connections onto neurons of the deep layers. They have further discovered that pharmacologically or optogenetically silencing activity in the upper cortical layers has no detectable impact on the activity of the deep layers. The thalamus appears to be independently driving activity in the upper and deeper halves of the cortex as if they are two separate systems. is conclusion is likely a general principle of the cerebral cortex—ranging from primary sensory areas, to high-level face and object recognition areas, to frontal executive regions—because all neocortical areas and mammalian species exhibit similar thalamocortical wiring.
Maitreya Dunham
University of Washington
David Prober +
California Institute of Technology

David Prober

RELATED STORY: David Prober: Sleeping Like the Fishes

David Prober (Milton E. Cassel Scholar)
Agata Smogorzewska
The Rockefeller University
Ye Zheng +
Salk Institute for Biological Studies

Ye Zheng

Ye Zheng earned his B.S. from Peking University in Beijing, China, and his Ph.D. from Columbia University. He was awarded a postdoctoral fellowship by the Cancer Research Institute to conduct research in Alexander Rudensky’s lab at the University of Washington in Seattle. After a brief sojourn as a research scholar at Memorial Sloan Kettering Cancer Center, he joined the Salk Institute for Biological Studies in 2009.

Regulatory T cells (Tregs) are a specialized subset of T cells that play a critical role in suppression of overexuberant immune response and maintenance of immune system homeostasis. Abnormal Treg function has been linked to multiple autoimmune diseases, such as arthritis, type 1 diabetes, lupus and multiple sclerosis, as well as inefficient tumor immunity. Research in the Zheng lab is focused on the molecular and cellular mechanisms of regulatory T cell development and function in the context of autoimmune and metabolic diseases. Foxp3, a member of the forkhead transcription factor family, is expressed specifically in regulatory T cells, and plays a pivotal role in Treg development and function. The Zheng lab discovered an intronic enhancer, named CNS2, at the Foxp3 genomic sequence, which is a “signal hub” for protection of Treg identity. They found that the activation of Tregs is a key event that triggers CNS2:promoter looping activity to stabilize Foxp3 expression. In addition to Tregs’ role in preventing autoimmune diseases, the Zheng lab recently revealed that Tregs are also involved in the development of metabolic diseases. They demonstrated that accumulation of adipose tissue resident Tregs is associated with insulin resistance in aged mice. This study highlighted a novel role of the immune compartment in contributing to key aspects of adipose health and disease.

2009

Ben E. Black +
Perelman School of Medicine at the University of Pennsylvania

Ben E. Black

Following undergraduate studies at Carleton College, Ben Black did a Ph.D. dissertation at the University of Virginia on pathways for nuclear protein export in the lab of Bryce Paschal. After a four-year postdoctoral fellowship with Don Cleveland in the Ludwig Institute for Cancer Research at the University of California, San Diego, Black started his own group at UPenn to continue the work he had started in the area of chromosome biology. Perhaps his best known work as an independent investigator is uncovering the physical basis for how nucleosomes containing the histone variant CENP-A epigenetically mark centromere location on the chromosome, and helping elucidate how these nucleosomes can seed new centromere assembly and maintain centromere location through a cell cycle-coupled self-propagation mechanism ultimately required to guide faithful chromosome inheritance. He has been recognized for his work with a fellowship from the American Cancer Society, a Career Award in the Biomedical Sciences from the Burroughs Wellcome Fund, and the Michael S. Brown New Investigator Award.

Over the last 10 years, the Black lab has contributed strongly to the chromosome field with discoveries in the following areas: (1) Rough biochemical and structural studies, defining the epigenetic mark that specifies the location on the chromosome of the centromere, which, in turn, confers the faithful inheritance of the chromosome at cell division (2) Elucidating the chromatin assembly pathway that epigenetically propagates centromere identity (3) Providing the genetic proof that centromere identity through the mammalian female germ line (>1 year in mice) relies upon spectacular stability of the special centromere-specifying nucleosome (4) Making key advances in the regulation of the master mitotic kinase, Aurora B (5) Important findings utilizing hydrogen/deuterium coupled to mass spec with several diverse chromatin complexes.
Jeremy S. Dittman
Weill Cornell Medical College
Aaron D. Gitler +
Stanford University School of Medicine (University of Pennsylvania)

Aaron D. Gitler

Aaron Gitler earned his B.Sc. in biochemistry and molecular biology from The Pennsylvania State University. He earned his Ph.D. in cell and molecular biology at the University of Pennsylvania, where he studied endothelial cell signaling pathways in cardiovascular development with Jonathan Epstein. He performed postdoctoral research at the Whitehead Institute for Biomedical Research and the Massachusetts Institute of Technology with Susan Lindquist until 2007, when he joined the faculty of the University of Pennsylvania in the Department of Cell and Developmental Biology. In 2012 he moved to the Stanford University School of Medicine.

Gitler’s research goal is to discover the cellular and molecular mechanisms by which protein aggregates contribute to neurodegeneration, and to harness these mechanisms to devise novel therapeutic strategies. His laboratory uses the baker’s yeast Saccharomyces cerevisiae as a simple, yet powerful, model system to study the cell biology underpinning protein-misfolding diseases, which include Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS). They have recently focused on the ALS disease proteins TDP-43, FUS/TLS and C9orf72, and have generated yeast models to define mechanisms by which these proteins contribute to ALS. They have used these yeast models to perform high-throughput, genome-wide modifier screens to discover suppressors and enhancers of toxicity. Launching from the studies in yeast, they have extended findings into animal models, and even into human patients. For example, Gitler and his collaborators discovered mutations in one of the human homologs of a hit from the yeast TDP-43 modifier screen, ataxin 2, in ALS patients, as a relatively common genetic risk factor for ALS. In recent work, they have pursued translational approaches to test whether some of the modifier genes from the yeast screens could be therapeutic targets for ALS and related diseases.
Steve Prescott +
University of Toronto (University of Pittsburgh)

Steve Prescott

Steve Prescott (Award in Pain Recipient) obtained his M.D. and Ph.D. degrees from McGill University in 2005. His doctoral research focused on the investigation of pain processing using electrophysiology, pharmacology and cellular imaging. He did postdoctoral training in computational neuroscience at the Salk Institute for Biological Studies with Terry Sejnowski. In 2008 he set up his own lab at the University of Pittsburgh with the intent of combining a range of experimental and computational tools to investigate pain processing. In 2012 his lab moved to The Hospital for Sick Children in Toronto. Prescott was named a Mallinckrodt Scholar and has also received a Canadian Institutes of Health Research New Investigator Award and an Ontario Early Researcher Award. He has received funding from the National Institutes of Health, the Canadian Institutes of Health Research, and the Natural Sciences and Engineering Research Council of Canada.

Trained as a clinician, experimentalist and theoretician, Prescott has a longstanding interest in the biophysics of information processing, especially in connection with neurological disease. His lab combines experiments (electrophysiology, optogenetics, calcium imaging, etc.) with computer simulations and mathematical analysis to uncover how changes in neuronal excitability and synaptic transmission affect neural coding. He is particularly interested in deciphering the nonlinear, systems-level basis for complex phenomena. In this context, his team has demonstrated how pathological changes in neuronal excitability implicated in neuropathic pain can arise through distinct molecular mechanisms; because multiple molecular changes that are individually sufficient to disrupt excitability are induced by nerve injury, no single molecular change is uniquely necessary for injury-induced excitability changes. This so-called degeneracy has important implications for choosing effective drug targets and may help explain why neuropathic pain is so difficult to treat. Moving forward, the lab is testing a theory of combinatorial coding, which posits that somatosensory information is encoded by the combination of cell types coactivated by different stimuli. They also study how neuronal excitability is homeostatically regulated and how distinct neural coding strategies are biophysically implemented.
Theodore Price +
The University of Texas at Dallas (University of Arizona)

Theodore Price

Theodore Price (Award in Pain Recipient) completed his Ph.D. at The University of Texas Health Science Center in San Antonio and a postdoctoral fellowship at McGill University. He took his first faculty position at the University of Arizona in 2007 and moved to UT Dallas in 2014, where he also directs the undergraduate neuroscience program and the Center for Advanced Pain Studies. Funded by the National Institutes of Health, Price’s laboratory focuses on molecular mechanisms involved in pain plasticity, with the goal of developing new therapeutics to reverse chronic pain states in humans. He has published more than 90 papers in leading journals, and has received early-career scholar awards from the American Pain Society and the International Association for the Study of Pain. Price is a member of the Somatosensory and Pain Systems Study Section of the NIH and serves on the editorial boards of numerous journals, including PAIN and the European Journal of Pain, where he is the pharmacology section editor.

Chronic pain is a major clinical problem that can persist for decades, but no disease-modifying treatments are available. Price’s work has focused on understanding the phenotypic changes that occur after injury that cause pain-sensing neurons to become hyperactive, driving chronic pain. His recent work has focused on how translation control signaling governs these phenotypic changes, which mRNAs are translated in an activity-dependent fashion in these neurons, and how targeting kinases that regulate translation of mRNAs can lead to disease modification resulting in long-lasting relief of chronic pain.
Samara Reck-Peterson +
University of California, San Diego (Harvard Medical School)

Samara Reck-Peterson

Samara Reck-Peterson (Milton E. Cassel Scholar)
Daniel B. Stetson +
University of Washington School of Medicine

Daniel B. Stetson

Daniel Stetson graduated with distinction from Duke University in 1997 and received his Ph.D. in 2002 from the University of California, San Francisco. After completing postdoctoral work at Yale University, Stetson joined the University of Washington Department of Immunology in April 2008. He has received a Cancer Research Institute Postdoctoral Fellowship and a National Institutes of Health Pathway to Independence Award. He was also named a Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Disease.

Research in the Stetson lab focuses on mechanisms by which cells detect and respond to viral infection. All organisms have viral pathogens, and all organisms have sensors that detect foreign nucleic acids. In vertebrates, these sensors coordinate an inducible antiviral response by activating the production of type I interferons (IFNs). While the pleiotropic roles of IFNs have been studied since their discovery almost six decades ago, recent advances have allowed scientists to understand their means of induction and complex regulation in molecular detail. Stetson’s research program seeks to understand the induction and regulation of antiviral responses. He studies these responses in the context of protective immunity and human autoimmune diseases.
Sohail Tavazoie
The Rockefeller University

2008

Steven J. Altschuler +
University of California, San Francisco (The University of Texas Southwestern Medical Center)

Steven J. Altschuler

Steven Altschuler (Milton E. Cassel Scholar) came to biology by way of pure mathematics, computer science and electrical engineering. He obtained an undergraduate degree in mathematics from the University of Pennsylvania and a Ph.D. under Richard Hamilton at the University of California, San Diego, working at the intersection of differential geometry, topology and nonlinear partial differential equations. With his longtime collaborator Lani Wu, Altschuler left the mathematics faculty at Princeton University to join the fledgling research division at Microsoft, where they founded a number of research efforts, including projects in video compression, semantic search, and speech/noise separation from multi-microphone input. Prior to arriving at UCSF, Altschuler and Wu were at Rosetta Informatics, fellows at the Bauer Center for Genomics Research at Harvard University, and associate professors at The University of Texas Southwestern Medical Center.

In their joint lab, Altschuler and Wu make use of experiment, quantitative data analysis, modeling and theory to investigate fundamental questions about the origins and impact of cellular heterogeneity in cellular decision-making, tissue development and homeostasis. Results from these studies are applied to investigate mechanisms of drug resistance, cancer evolution and new therapeutic strategies. The lab investigates fundamental questions about the origins and impact of cell-to-cell differences in the context of homeostatic tissue maintenance of healthy tissue and deregulation of diseased states. A common theme is the combined use of single-cell perturbation assays, quantitative imaging, data-driven modeling and theory, which is empowered by a multidisciplinary approach and team. Through the lens of cellular heterogeneity, the lab investigates the development of complex tissues (systems biology), disease progression (cancer systems biology) and drug discovery (systems pharmacology).
Paul Chang
ARase Therapeutics (Massachusetts Institute of Technology)
Ian J. Davis +
The University of North Carolina at Chapel Hill

Ian J. Davis

As an undergraduate at Northwestern University, Ian Davis was first introduced to molecular biology while working in the labs of Richard Morimoto at Northwestern and Steven Heniko at the Fred Hutchinson Cancer Research Center. He then went on to graduate studies in mammalian genetics with Lester Lau at the University of Illinois at Chicago. Following completion of his M.D. from Northwestern University Medical School, he served as a resident and then chief resident in pediatrics at Boston Children’s Hospital. He then completed subspecialty training in pediatric hematology/oncology at Dana-Farber Cancer Institute and Boston Children’s Hospital, during which time he did postdoctoral studies with David Fisher. In 2006 he joined the faculty of the University of North Carolina at Chapel Hill, where he is currently an attending physician in pediatric hematology/oncology, affiliated with the Lineberger Comprehensive Cancer Center, the program in Chromatin and Epigenetics, and the Carolina Center for Genome Sciences, and holds the G. Denman Hammond Associate Professorship for Childhood Cancer. In addition to a Rita Allen Foundation award, Davis received a Martin D. Abelo Scholar Award from the V Foundation for Cancer Research.

The Davis lab has been interested in the way that proteins and DNA interact in the nucleus to control gene expression and influence cancer development. Supported by hypothesis-driven computational analytics that enable the integration of genome-wide assays of chromatin accessibility, histone post-translational modification and transcriptomics, the lab has focused on the childhood and young adult bone tumor Ewing sarcoma and clear cell renal cell carcinoma. Major projects in the lab include exploration of the role of altered histone post-translational modifications in cancer, and the use of chromatin accessibility to explore the mechanisms of aberrant transcription and to identify novel chemical probes and epigenetically targeted therapies.
Ming Li +
Memorial Sloan Kettering Cancer Center

Ming Li

Ming Li received a B.S. in biochemistry from Fudan University in Shanghai, China, and an M.S. in molecular biology from the Shanghai Institute of Biochemistry. After obtaining a Ph.D. degree in immunology at Columbia University, Li joined Richard Flavell’s lab at Yale University as a postdoctoral fellow. In 2007 Li started his lab at Memorial Sloan Kettering Cancer Center. In addition to a Rita Allen Foundation Award, Li has received an American Cancer Society Scholar grant, a Louise and Allston Boyer Investigator Award for Basic Research, a Leukemia and Lymphoma Society Scholar award and an AAI-BD Biosciences Investigator Award from the American Association of Immunologists.

Studies from Li’s laboratory have led to the elucidation of regulatory mechanisms of T cell development, homeostasis, tolerance and memory, as well as mechanisms of T cell regulation in cancer. His research group showed that the evolutionarily conserved TGF-beta and Foxo signaling pathways regulate thymic T cell selection and differentiation. TGF-beta signaling also endows low-affinity T cells with homeostatic properties during thymic selection, while Foxo proteins control the survival and trafficking of naïve T cells in peripheral lymphoid organs. Furthermore, Li’s team demonstrated that TGF-beta and Foxo pathways are pivotal regulators of tolerance by direct and indirect suppression of autoreactive T cells. Using oncogene-driven experimental models of cancer, they showed that TGF-beta signaling in T cells represses antitumor immunity, which is mediated by T cell-derived but not tumor-produced TGF-beta. His lab’s most recent work revealed a distinct lineage of tumor-associated macrophages that arise from inflammatory monocytes through Notch-dependent mechanisms and promote T cell tolerance to tumors. Together, these studies have unraveled the repurposing of ancient TGF-beta, Foxo and Notch signaling pathways for the regulation of highly specialized T cell activities in health and cancer. These discoveries have also established the concept of evolutionary co-option working in concert with innate and adaptive recognition to control immune pathophysiology.
Emmanuelle A. Passegué +
Columbia University Medical Center (University of California, San Francisco)

Emmanuelle A. Passegué

Emmanuelle Passegué earned her Ph.D. in endocrinology, summa cum laude, from the University of Paris XI. She was a postdoctoral fellow at the Institute of Molecular Pathology in Vienna, Austria, from 1996 to 2000, and then joined the Department of Pathology at Stanford University, where she served as a postdoctoral fellow and a research associate. She was a faculty member in the Department of Medicine at the University of California, San Francisco, from 2005 to 2017, when she moved to Columbia University Medical Center, where she directs the Columbia Stem Cell Initiative. In addition to the Rita Allen Foundation Scholar award, she has been honored with the Jose Carreras International Leukemia Foundation Postdoctoral Fellowship, the American Society of Hematology Scholar Award, the California Institute for Regenerative Medicine New Investigator Award, the Leukemia and Lymphoma Society Scholar Award, the International Society of Experimental Hematology’s McCulloch and Till Lectureship Award, and the Glenn Award for Research on the Biological Mechanisms of Aging.

She is widely recognized for her expertise on hematopoietic stem cell (HSC) biology. Her research over the past 10 years has focused on understanding the cellular and molecular processes controlling HSC activity during homeostasis, and addressing how these regulations are changed in myeloid malignancies and physiological aging. The goal of her research is to identify affected genes and/or pathways that can be used to develop new therapies to treat human diseases. Toward this end, her team is employing a variety of cross-disciplinary approaches using mouse models and human patient samples. Current projects in the laboratory investigate the role of apoptosis, autophagy, immune regulations, DNA repair mechanisms, and changes in the bone marrow niche microenvironment in HSC function in normal and deregulated conditions.
E. Alejandro Sweet-Cordero
Stanford University Medical School

2007

Michael T. Hemann +
Massachusetts Institute of Technology

Michael T. Hemann

Michael Hemann received his B.A. in molecular biology and biochemistry from Wesleyan University and his Ph.D. in human genetics from Johns Hopkins University, where he worked with Carol Greider. He was a postdoctoral fellow at Cold Spring Harbor Laboratory in the laboratory of Scott Lowe, a 1999 Rita Allen Foundation Scholar (now at Memorial Sloan Kettering Cancer Center). Hemann’s research focuses on identifying new approaches to improve conventional and targeted anticancer therapeutics. He is the recipient of the Harold M. Weintraub Graduate Student Award (which honors the 1976 Rita Allen Foundation Scholar, who passed away in 1995) and was a Helen Hay Whitney Fellow. Hemann is a codirector of the MIT graduate program in biology.

Many human cancers fail to respond to traditional therapeutics due to acquired drug resistance. The mechanism of this chemo-resistance has yet to be fully elucidated, and thus poses a major hurdle in the effectiveness of cancer therapies. Hemann’s group uses cutting-edge genetic tools combined with mouse tumor transplantation systems to study tumor progression and the role that individual genes and combinations of genes play in drug resistance. This approach not only has the potential to identify novel targets for effective therapies, but can also be used to help modify traditional therapies to be more effective against typically resistant cancers.
Tae Hoon Kim +
The University of Texas at Dallas (Yale University School of Medicine)

Tae Hoon Kim

RELATED STORY: Tae Hoon Kim: Searching for the Genome’s Switches and Dials

Tae Hoon Kim obtained a bachelor’s degree from Reed College and a Ph.D. in biochemistry from Harvard University under the tutelage of Tom Maniatis, a 1978 Rita Allen Foundation Scholar and a pioneer of molecular cloning. He completed postdoctoral training in genomics with Bing Ren, an international leader of functional genomics, at the Ludwig Institute for Cancer Research at the University of California, San Diego. In 2006 Kim joined the faculty of the Yale University School of Medicine. In 2014 he moved to the University of Texas at Dallas. Kim has devoted his research career to understanding transcriptional regulation of the human genome, and has been pioneering techniques for global analyses of protein-DNA interactions. His technical and research accomplishments have been recognized nationally by a number of private foundations and by the National Institutes of Health. In addition to a Rita Allen Foundation award, he has received a Ruth L. Kirschstein National Research Service award, a Sidney Kimmel Scholar award, and an Alexander and Margaret Stewart Trust fellowship.

Over the past several years, the Kim laboratory has contributed to understanding of transcriptional and epigenetic control of the human genome by uncovering and examining new and emerging gene control mechanisms relevant for health and disease, and by pioneering new functional genomics approaches. They have been characterizing a key class of cis-regulatory elements known as insulators, which function in higher-order folding of the chromosomes into a 3-D genome to facilitate transcription insulation. They determined the distribution of the insulator protein CTCF across the human genome, identified the recognition sequence responsible for its distribution across vertebrate genomes, and proposed a possible mode of evolution of its binding sites. From this analysis, Kim’s group identified recruitment of the chromosomal protein cohesin as a novel mechanism for regulating topological segregation of heterochromatin at chromatin boundaries. They also identified a long noncoding RNA involved in maintaining topological segregation of heterochromatin. In parallel, their analysis of global nascent transcription in the human genome is allowing them to identify and characterize novel enhancers and associated long noncoding RNAs that function to regulate target gene expression in innate immunity and in cancers.
Lloyd C. Trotman +
Cold Spring Harbor Laboratory

Lloyd C. Trotman

RELATED STORY: Lloyd Trotman: Transforming Views of Prostate Cancer

Lloyd Trotman earned his M.S. in biochemistry and his Ph.D. in cell biology from the University of Zurich. He was a postdoctoral fellow at Memorial Sloan Kettering Cancer Center, and joined Cold Spring Harbor in 2007. He has received the Pershing Square Sohn Prize for Young Investigators in Cancer Research from Pershing Square Sohn Cancer Research Alliance and the American Society for Cell Biology’s Merton R. Bernfield Memorial Award. He also has been named an American Cancer Society Scholar and a V Foundation Scholar. His research has been supported by a Department of Defense (DOD) Prostate Cancer Idea Award, a DOD Prostate Cancer Research Program New Investigator Award, a V. Kann Rasmussen Foundation Award and a Starr Cancer Consortium Grant Award.

With more than 200,000 U.S. cases per year, prostate cancer is the most commonly diagnosed malignancy in men and the second most common cause of male cancer deaths. Trotman’s lab aims to understand lethal prostate cancer and to speed up the search for a cure. While progress in clinical research is naturally limited by the established standards of care, therapy using animal models is not. Model therapy, in contrast, is limited by the qualities of the model system. Based on their analysis of human cancer genomes, Trotman and his team have generated a first-in-kind mouse model for tracking of endogenous metastatic prostate cancer, termed RapidCaP. This system allows for live visualization of metastasis and therapy failure and for molecular/genetic dissection of these processes.
Mark J. Zylka +
The University of North Carolina at Chapel Hill

Mark J. Zylka

RELATED STORY: Connecting the Causes of Pain and Childhood Neurological Disorders

Mark Zylka (Milton E. Cassel Scholar)

2006

Joshua T. Mendell +
The University of Texas Southwestern Medical Center (Johns Hopkins University School of Medicine)

Joshua T. Mendell

RELATED STORY: Joshua Mendell: Drawn to the Enigmas of RNA
Peter W. Reddien +
Massachusetts Institute of Technology

Peter W. Reddien

Peter Reddien (Milton E. Cassel Scholar)
Adrian Salic +
Harvard Medical School

Adrian Salic

RELATED STORY: Adrian Salic: How Cells Sense the Body’s Plan

Adrian Salic obtained his Ph.D. from Harvard University, working on the biochemistry of Wnt signaling, a key cell-to-cell signaling pathway involved in colon cancer. He then conducted postdoctoral studies in the Department of Systems Biology at Harvard Medical School, during which he focused on how a cell’s genetic material is equally divided between its daughter cells.

Salic’s lab has two main interests: 1) understanding the molecular mechanisms involved in cell-to-cell signaling through the Hedgehog pathway, which plays fundamental roles in development and cancer; and 2) developing novel chemical probes for microscopic imaging and functional assays of various biological molecules (nucleic acids, proteins, lipids) in cells and in animals.

2005

Hilary A. Coller +
University of California, Los Angeles (Princeton University)

Hilary A. Coller

RELATED STORY: Hilary Coller: When Cells Sleep

Hilary Coller (Milton E. Cassel Scholar) received her undergraduate degree in biochemistry and molecular biology from Harvard University. She received a Ph.D. in toxicology from the Massachusetts Institute of Technology, where she studied the role of environmental chemicals as mutagenic agents in human tissue. She did postdoctoral training at the Whitehead/MIT Center for Genome Research in the laboratories of Eric Lander and Todd Golub, and at the Fred Hutchinson Cancer Research Center in the laboratory of Jim Roberts. Coller is an associate editor of Physiological Genomics and leads the Systems Biology of Cell State Regulation Theme for the journal. At UCLA, she chairs the Bioinformatics-IDP Outreach Committee.

Coller’s research has focused on understanding the molecular basis for the functional characteristics of the cellular state of quiescence, or reversible cell cycle arrest. Her research has overturned the commonly held perception of quiescence as a “sleepy” or default state, and shown that quiescence is an active and highly regulated process. In a model system involving primary human diploid fibroblasts, her group discovered that quiescent cells activate the Notch signaling pathway, and that the Notch transcription factor Hes-1 actively protects them from irreversible cell cycle states such as differentiation and senescence. The Coller laboratory discovered that cell cycle arrest with quiescence is not a default state, but rather is actively maintained by microRNAs and histone modifications that enforce cell cycle exit. Knocking down specific microRNAs or a histone methyltransferase resulted in increased cell proliferation. They also discovered that quiescent, but not proliferating, fibroblasts actively engage the pentose phosphate pathway to protect themselves from an accumulation of oxidative damage and apoptosis. There is a debate in the scientific community about whether quiescence represents a distinct state, and Coller’s findings defining a pathway that is relied upon by quiescent cells, but dispensable in proliferating cells, demonstrate that quiescence is a distinct state.
Elsa R. Flores +
Moffitt Cancer Center (The University of Texas MD Anderson Cancer Center)

Elsa R. Flores

RELATED STORY: Elsa R. Flores: Pursuing New Pathways to Foil Cancer

Elsa Flores received her B.S. in chemical engineering from the Massachusetts Institute of Technology and her Ph.D. in cancer biology from the University of Wisconsin-Madison. She did a postdoctoral fellowship, sponsored by the Leukemia & Lymphoma Society of America, in Tyler Jacks’ laboratory at MIT. In his lab, she found that p63 and p73 are required for p53-dependent apoptosis in response to DNA damage, and that p63 and p73 are tumor suppressor genes. Recent work in her laboratory includes deciphering the functions of the TA and ΔN isoforms of p63 and p73 in multiple biological processes using conditional knockout mouse models to target the p53 pathway in cancer therapeutically. Flores is a National Cancer Institute Outstanding Investigator and has received awards from the American Cancer Society and the V Foundation for Cancer Research, in addition to the Rita Allen Foundation. In September 2016 she became Co-Leader of the Cancer Biology and Evolution Program and Chair of Molecular Oncology Department at the Moffitt Cancer Center in Tampa, Florida.

Many genes with driver mutations in cancer are members of gene families. The existence of redundant functions in gene families has made diseases like cancer challenging to treat and cure due to limited knowledge about the functions of each gene within the family. The p53 family is one such gene family. Despite long-standing knowledge that p53 function is frequently altered in cancer, p53 has persisted as an “undruggable” target because of its function as a transcription factor and because it lacks an enzymatic activity that can be readily inhibited. In an effort to identify novel ways of targeting p53 in cancer, the Flores laboratory has been focused on understanding the interrelated biological functions of the p53 family, which includes the p63 and p73 genes. They have identified novel functions for p63 and p73 in metastasis, miRNA biogenesis, long noncoding RNA regulation, stem cell maintenance and metabolism using novel mouse models. These mouse models have also revealed novel functions of p63 and p73 in tumor metabolism and have allowed the manipulation of particular isoforms of p63 and p73 to therapeutically target p53-deficient and mutant tumors.
Johanna Joyce +
University of Lausanne (Memorial Sloan Kettering Cancer Center)

Johanna Joyce

RELATED STORY: Johanna Joyce: Fighting Tumors Through Cellular “Reeducation”
Joel L. Pomerantz +
Johns Hopkins University School of Medicine

Joel L. Pomerantz

RELATED STORY: Joel Pomerantz: Immunity’s Molecular Dance

2004

Laura A. Johnston +
Columbia University Medical Center

Laura A. Johnston

RELATED STORY: Laura Johnston: How Life Shapes Up

Laura Johnston received a B.S. in biology from Pacific Lutheran University and a Ph.D. in molecular pathology from the University of Washington. She conducted postdoctoral research in the laboratory of Bruce Edgar (a 1995 Rita Allen Foundation Scholar) at the Fred Hutchinson Cancer Research Center in Seattle. She joined the faculty of Columbia University Medical Center in 2000, and was named Professor of Genetics and Development in 2016. She is the president-elect of the National Drosophila Board of Directors.

The Johnston laboratory investigates the mechanisms used by growing tissues to gauge the collective and individual fitness of cells and thereby optimize tissue and animal fitness. Johnston’s team is interested in basic biological mechanisms and also in their relevance to developmental and tumorigenic pathologies. They use the simple genetic model organism Drosophila and have developed tools and strategies that allow manipulation of growth and cell fitness in living, growing animals. Projects include: investigation of the role of the conserved oncogene and growth regulator Myc in mediation of cooperative and competitive interactions during tissue and organ growth; investigation of homeostatic processes, including metabolism, that allow cells to sense and respond to growth changes in their immediate environment; roles of p53, Toll receptors and NFkB as sensors and effectors of cellular fitness; and molecular genetic dissection of tissue regeneration. These processes provide plasticity to growing organs, and the Johnston lab is addressing their importance in normal growth, during regeneration and as mechanisms that may be exploited by precancerous cells during tumor progression.
Senthil K. Muthuswamy +
Harvard Medical School (Cold Spring Harbor Laboratory)

Senthil K. Muthuswamy

RELATED STORY: Senthil Muthuswamy: Tackling Cancer in Three Dimensions
David M. Sabatini +
Massachusetts Institute of Technology

David M. Sabatini

RELATED STORY: David Sabatini: Fueling Cell Growth
David A. Tuveson +
Cold Spring Harbor Laboratory (University of Pennsylvania)

David A. Tuveson

RELATED STORY: David Tuveson: Decoding a Cryptic Cancer

In addition to holding positions at Cold Spring Harbor Laboratory, David Tuveson is the Director of Research for the Lustgarten Pancreatic Cancer Research Foundation, and he cares for pancreatic cancer patients at Memorial Sloan Kettering Cancer Center. He received his medical and graduate training at the Johns Hopkins University School of Medicine, followed by clinical training at Brigham and Women’s Hospital and Dana-Farber/Harvard Cancer Center. While at Dana-Farber,Tuveson codeveloped imatinib with George Demetri for gastrointestinal stromal tumor patients. Following postdoctoral training with Tyler Jacks at MIT, Tuveson directed laboratories at the University of Pennsylvania and the University of Cambridge prior to moving to Cold Spring Harbor in 2012.

His research team established mouse models of pancreatic cancer to explore the biology of the disease and identify new therapeutic and diagnostic approaches. They created several therapeutic opportunities regarding stromal targeting that are now undergoing clinical evaluation. Most recently, they developed murine and human organoid models of pancreatic cancer to expedite fundamental and applied research.
Zheng Zhou +
Baylor College of Medicine

Zheng Zhou

Zheng Zhou earned her B.S. from Fudan University in Shanghai, China, and her Ph.D. from Baylor College of Medicine. She completed postdoctoral training at the Massachusetts Institute of Technology, and then returned to Baylor as a faculty member. She also serves as an adjunct faculty member at Rice University. She received postdoctoral fellowships from the Cancer Research Fund of the Damon Runyon-Walter Winchell Foundation and the Merck/MIT Collaboration Program. She has also been honored with an Investigator Award of the Cancer Research Institute and a Basil O’Connor Starter Scholar Research Award of the March of Dimes Birth Defect Foundation.

Zhou’s laboratory studies the mechanisms of dying cell clearance. During animal development and in adulthood, cells undergoing apoptosis are rapidly internalized by other cells via phagocytosis (engulfment) and degraded inside phagocytes. The phagocytic removal of dying cells is an evolutionarily conserved process that has important physiological impacts. The removal of apoptotic cells provides a safe means for eliminating unwanted and dangerous cells from the body. It prevents tissue injury, inflammatory responses and autoimmune responses that could be induced by the content of dead cells. In addition to apoptotic cells, cells that die through necrosis, another type of cell death frequently caused by acute injury and morphologically distinct from apoptosis, are also removed via phagocytosis. The removal of necrotic cells, which are associated with neurodegenerative disorders and stress responses, is considered critical for tissue regeneration. The study of the dying cell removal process is also closely related to cancer research and treatment. Zhou’s laboratory investigates the conserved molecular mechanism that controls the recognition, engulfment and degradation of dying cells, using the nematode C. elegans as a model organism.

2003

Ajay Chawla +
University of California, San Francisco (Stanford University School of Medicine)

Ajay Chawla

RELATED STORY: Ajay Chawla: Beyond Immunity
Leslyn A. Hanakahi
University of Illinois at Chicago (Johns Hopkins University)
Christopher Lima +
Memorial Sloan Kettering Cancer Center (Weill Cornell Medical College)

Christopher Lima

RELATED: Christopher Lima: Structure Meets Function
Shai Shaham
The Rockefeller University

2002

Mark Henkemeyer
The University of Texas Southwestern Medical Center
Xianxin Hua +
Perelman School of Medicine at the University of Pennsylvania

Xianxin Hua

Xianxin Hua earned M.S. and M.D. degrees from Wuhan Medical College Yunyang School in Shiyan, China. He received a Ph.D. in cell regulation from The University of Texas Southwestern Medical Center, where he worked with Joseph Goldstein and Michael Brown. Hua was a postdoctoral fellow and clinical scientist in the laboratory of HarveyLodish at the Whitehead/MIT Center for Genome Research. In 2000 he joined the faculty of the University of Pennsylvania School of Medicine. He has received multiple awards for his research, including a Burroughs Wellcome Career Award and a Harrington Scholar-Innovator award in addition to a Rita Allen Foundation award.

Hua’s group is interested in dissecting the function of menin, which is mutated in the hereditary human tumor syndrome multiple endocrine neoplasia type 1 (MEN1), in repressing pancreatic beta cells and endocrine tumors and in promoting leukemogenesis. This line of research is crucial because menin is a master regulator in controlling the population of endocrine cells, including insulin-secreting beta cells as well as hematopoietic cells, which generate blood cells that can transform into leukemia. First, the Hua lab seeks to elucidate how menin suppresses endocrine cells, such as pancreatic beta cells, via regulating histone methylation and expression of pro-proliferative genes. They are also interested in identifying menin-regulated key pathways that can be suppressed to inhibit neuroendocrine tumors. Moreover, they will determine how menin, which acts as a tumor promoter in MLL fusion protein-induced leukemia, cooperates with wild-type MLL protein to promote leukemia, and how the menin and wild-type MLL axis can be suppressed to improve therapy for this aggressive leukemia. Finally, it is important to understand how inhibition of menin leads to reversal of established diabetes, as menin is a key pro-diabetic factor in beta cells, and especially in stressed islets in diabetic patients. These comprehensive approaches will provide novel insights into the molecular mechanisms for MEN1 tumorigenesis, regulation of beta cells and leukemogenesis, shedding light on improving therapy against neuroendocrine tumors, leukemia and diabetes.
William Talbot
Stanford University School of Medicine
Hao Wu +
Harvard Medical School (Weill Cornell Medical College)

Hao Wu

RELATED STORY: Hao Wu: The Cellular Dimensions of Immunity

2001

Steven Artandi +
Stanford University School of Medicine

Steven Artandi

Steven Artandi earned his A.B. in chemistry from Princeton University, and his M.D. and Ph.D. in microbiology from Columbia University. He completed his residency at Massachusetts General Hospital and a clinical fellowship in medical oncology at Harvard University, Dana Farber Cancer Institute, Brigham and Women’s Hospital and Massachusetts General Hospital. He also had a research fellowship at Dana Farber and Harvard. In 2000, he joined the faculty at Stanford. He has received a Howard Hughes Medical Institute Postdoctoral Research Fellowship for Physicians, a National Institutes of Health K08 Grant, a V Foundation Scholar Grant, a Pfizer/American Federation for Aging Research Innovations in Aging Research Grant, and a Glenn Award for Research in Biological Mechanisms of Aging. Artandi has served as senior editor and on the editorial board of Molecular Cancer Research, as well as on the editorial board of Stem Cells. He was elected a fellow of the American Association for the Advancement of Science in 2007 and received the National Cancer Institute Outstanding Investigator Award in 2015.

The human aging process makes us prone to cancer and to degenerative diseases. The Artandi lab uses sophisticated biochemical, cell biological and genomic approaches to understand the fundamental causes of these diseases. Their goal is to develop new therapeutic approaches to tackle these often-intractable disease states. Their research focuses on four areas: 1) Telomeres and human disease—the impaired function of telomeres (the caps that protect chromosome ends) occurs with normal aging and in settings of disease. Telomere dysfunction impairs tissue regeneration and blocks cancer development. Artandi and his colleagues seek to understand how this process influences degenerative disease and cancer. 2) Tissue homeostasis and regeneration—maintenance of many tissues fails with advanced aging and disease. They study the underlying mechanisms governing tissue homeostasis and repair. 3) The origins of cancer—the cellular origins of cancer remain largely mysterious. They study the early stages of human carcinogenesis and how cancers acquire cellular immortality. 4) Telomerase function in cancers and stem cells—the telomerase enzyme lengthens telomeres, a critical step in cellular immortality. They seek to understand how telomerase functions inside living human cells.
David C. Chan
California Institute of Technology
Adrian R. Ferre-D’Amare
National Heart, Lung, and Blood Institute (Fred Hutchinson Cancer Research Center)
Oliver Hobert
Columbia University
Daniel L. Minor, Jr. +
University of California, San Francisco

Daniel L. Minor, Jr.

Daniel Minor, Jr. received a B.A. in biochemistry and biophysics from the University of Pennsylvania and a Ph.D. in chemistry from the Massachusetts Institute of Technology, where he worked with Peter Kim, a 1990 Rita Allen Foundation Scholar. He conducted postdoctoral research with Nigel Unwin at the Medical Research Council Laboratory of Molecular Biology in Cambridge, England, and with Lily Jan at the University of California, San Francisco. He joined the faculty of UCSF in 2000. In addition to a Rita Allen Foundation award, Minor has received Alfred P. Sloan Research Fellow, Beckman Young Investigator, Searle Scholar and McKnight Technological Innovations in Neuroscience awards. He has been selected as an Established Investigator of the American Heart Association and a fellow of the American Asthma Foundation.

Ion channels are fundamental components of biological electrical signaling networks. These proteins control the passage of ions across the cell membrane and generate the bioelectricity that is essential for life. Much of the future of neuroscience, cardiovascular research and design of biomimetic membrane systems lies in understanding the molecular details of how these protein machines function, how they are regulated and how they are integrated into large, macromolecular complexes within the cell. Minor’s laboratory seeks to uncover the basic mechanisms by which ion channels act. His team uses a multidisciplinary approach that includes genetic selections, X-ray crystallography, cryo-electron microscopy, solution biophysical methods, small-molecule screening and electrophysiology. They are interested in understanding the high-resolution structures of channel proteins, their regulatory factors, and the conformational changes that accompany channel action, as well as in the development of novel means to manipulate channel action in vivo.

2000

Yukiko Goda
RIKEN Brain Science Institute (University of California, San Diego; University College London)
Gregory J. Hannon +
Cancer Research UK Cambridge Institute (Cold Spring Harbor Laboratory)

Gregory J. Hannon

RELATED STORY: Gregory Hannon: Tools for Tough Questions

Gregory Hannon is Senior Group Leader of the CRUK Cambridge Institute and Professor of Molecular Cancer Biology and a Wellcome Trust Investigator at the University of Cambridge. He is a former Howard Hughes Medical Institute Investigator, an Associate Core Member and Director of Cancer Genomics at the New York Genome Center, and an Adjunct Professor at Cold Spring Harbor Laboratory. He obtained a B.A. in biochemistry from Case Western Reserve University and a Ph.D. in molecular biology from the same institution. His work focuses on the roles of small RNAs, the biology of cancer cells, and the mammalian genome as revealed through next-generation sequencing. Hannon received the 2007 National Academy of Sciences Award in Molecular Biology and the 2007 Paul Marks Prize for Cancer Research from Memorial Sloan Kettering Cancer Center. He was elected a member of the National Academy of Sciences in May 2012.
Michael P. Rout
The Rockefeller University
Samuel Wang +
Princeton University

Samuel Wang

An alumnus of the California Institute of Technology, where he received a B.S. with honor in physics, Samuel Wang went on to earn a Ph.D. in neuroscience from the Stanford University School of Medicine in 1994. He conducted postdoctoral research at Duke University and then Bell Labs Lucent Technologies. In the mid-1990s, he also worked on science and education policy for the U.S. Senate Committee on Labor and Human Resources. Wang joined the Princeton faculty in 2000. He is the recipient of National Science Foundation, W.M. Keck Foundation and Alfred P. Sloan Young Investigator Awards. He has written two books: Welcome to Your Brain: Why You Lose Your Car Keys But Never Forget How to Drive and Other Puzzles of Everyday Life, and Welcome to Your Child’s Brain: How the Mind Grows from Conception to College. Wang is also noted for developing statistical methods to analyze U.S. presidential election polls with unusually high accuracy. He is a member of the Rita Allen Foundation Board of Directors.

Wang’s research focuses on the cerebellum’s role in cognition and social thought processes, and he uses advanced imaging methods to search for clues to the causes of autism.

1999

Susan M. Dymecki +
Harvard Medical School

Susan M. Dymecki

RELATED STORY: Susan Dymecki: Serotonin Circuit Master

Susan Dymecki received her B.S.E. and M.S.E. from the University of Pennsylvania, and M.D. and Ph.D. from the Johns Hopkins University School of Medicine. After completing doctoral studies, Dymecki began independent work as a Helen Hay Whitney Fellow and John Merck Scholar at the Carnegie Institution of Washington, where she developed genetic approaches in mice to study the deployment and function of embryonic cell lineages as means to examine mammalian nervous system development. She joined the faculty of Harvard Medical School in 1998, became a Rita Allen Foundation Scholar in 1999, earned the HMS Morgan-Zinsser Teaching Faculty Fellowship Award and the Gulf Oil Outstanding Achievement in Biomedical Science Award, and received the Biological and Biomedical Sciences Ph.D. Program mentoring award—she now serves as director of this program.

Dymecki’s lab has pioneered transgenic tools to subtype neurons by molecular identity and probe each subtype’s function, connectivity and origin—as illustrated by her discoveries on the brain serotonergic system. Dymecki has identified numerous subtypes of serotonergic neurons and uncovered their network nodes and discrete functions, from respiratory to affective. Elucidating this heterogeneity brings insight into serotonin involvement in such diverse disorders as sudden infant death syndrome and depression, providing novel ways to conceptualize and potentially attack these intractable disorders.
K. Christopher Garcia
Stanford University School of Medicine
Scott W. Lowe
Memorial Sloan Kettering Cancer Center (Cold Spring Harbor Laboratory)
Yigong Shi +
Tsinghua University (Princeton University)

Yigong Shi

Yigong Shi received his bachelor’s degree with highest honor from Tsinghua University in 1989 and his Ph.D. in biophysics from the Johns Hopkins University School of Medicine in 1995. Following a postdoctoral fellowship at the Memorial Sloan Kettering Cancer Center, he joined Princeton University as an Assistant Professor in 1998 and was promoted to Professor in 2003. He was named the Warner-Lambert/Parke-Davis Professor of Molecular Biology in 2007. He resigned from Princeton University, declined an Investigator’s offer from Howard Hughes Medical Institute and returned to Tsinghua University in 2008. He is a foreign associate of the U.S. National Academy of Sciences, an honorary foreign member of the American Academy of Arts and Sciences, a fellow of the American Association for the Advancement of Science and a foreign associate of the European Molecular Biology Organization.

Shi’s research focuses on three distinct areas: programmed cell death, regulated intramembrane proteolysis, and pre-mRNA splicing. He has received a number of recognitions, including a 1999–2002 Searle Scholarship, the 2003 Irving Sigal Young Investigator Award from the Protein Society, the 2010 Sackler Prize in Biophysics, and the 2014 Gregori Amino Prize from the Royal Swedish Academy of Sciences.

1998

Frank J. Hsu
Immune Design (Yale University School of Medicine)
Peter Mombaerts +
Max Planck Research Unit for Neurogenetics (The Rockefeller University)

Peter Mombaerts

Peter Mombaerts obtained his M.D. from the Catholic University of Leuven. He then joined the laboratory of Susumu Tonegawa at the Massachusetts Institute of Technology, where he obtained his Ph.D. with a thesis on immunodeficient mice generated by gene targeting. As a postdoc with Richard Axel at Columbia University, he developed a genetic approach to visualize axonal projections of mouse olfactory sensory neurons that express the same odorant receptor gene. From 1995 to 2007 he was a faculty member at The Rockefeller University. In 2008 he moved to Frankfurt, Germany, as director of the newly created Department of Molecular Neurogenetics at the Max Planck Institute of Biophysics, and in 2013 he became the director of the independent Max Planck Research Unit of Neurogenetics. His research interests are the development and function of the mouse olfactory system, and his expertise is genetic manipulation of the mouse.
Ilaria Rebay
University of Chicago (Massachusetts Institute of Technology)
Jon S. Thorson
University of Kentucky (Memorial Sloan Kettering Cancer Center)

1996

Andrew Chess +
Icahn School of Medicine at Mount Sinai (Massachusetts Institute of Technology)

Andrew Chess

Andrew Chess received a B.S. from the Massachusetts Institute of Technology, where he studied biology and conducted research in Richard Mulligan’s lab. He then went to the Columbia University College of Physicians and Surgeons for his M.D. degree. During medical school, he also did research in Richard Axel’s lab and continued there for his postdoctoral work. Chess’ first faculty position was at the Whitehead Institute for Biomedical Research and the MIT Department of Biology. He then moved to Harvard Medical School and Massachusetts General Hospital. In 2010 he moved with his wife, psychiatrist and neuroscientist Pamela Sklar, to Mount Sinai.

During his postdoctoral work, and continuing in his own lab, Chess made a number of discoveries in the olfactory systems of catfish, mice and Drosophila. His lab’s work has been central in revealing that autosomal random monoallelic expression extends well beyond the allelic exclusion of T cell receptor and immunoglobulin genes, and is in fact a phenomenon that may influence up to 10 percent of the genome and may be an important determinant of adult phenotypes.

The Chess lab has studied DNA methylation, a crucial mode of epigenetic regulation important for normal development and tissue. For example, the lab was the first to demonstrate that gene-body methylation plays a role in gene regulation in animals. They also showed that genetic polymorphisms influence DNA methylation in cis, a potential mechanism for connecting genotypic diversity to phenotypic diversity. Studying alternative splicing of DSCAM in individual Drosophila neurons, they were the first to propose and provide evidence for the idea that alternative splicing can provide neurons with unique molecular identities.
Robert K. Ho
University of Chicago (Princeton University)
Li-Huei Tsai +
Massachusetts Institute of Technology (Harvard Medical School)

Li-Huei Tsai

Li-Huei Tsai received her Ph.D. degree from the University of Texas Southwestern Medical Center at Dallas. She completed her postdoctoral work with Edward Harlow’s laboratory at Cold Spring Harbor Laboratory and Massachusetts General Hospital. In 1994, Tsai joined the faculty in the Department of Pathology at Harvard Medical School and was named an Investigator of the Howard Hughes Medical Institute in 1997. In 2006, she was appointed Professor in the Department of Brain and Cognitive Sciences, and joined the Picower Institute for Learning and Memory at MIT. She has received several awards, including an Outstanding Contributor Award from the Alzheimer Research Forum, a Simons Foundation Autism Research Initiative Award, an NIH Cantoni Lecture Award and a Glenn Foundation Award for Research in Biological Mechanisms of Aging. She also has been named an Academician by Academia Sinica and is a fellow of the American Association for the Advancement of Science.

Tsai’s laboratory is interested in elucidating the pathogenic mechanisms underlying neurological disorders that impact learning and memory. They are taking a multidisciplinary approach to investigate the molecular, cellular and circuit basis of neurodevelopmental and neurodegenerative disorders.

1995

Stephen P. Bell
Massachusetts Institute of Technology
Titia de Lange +
The Rockefeller University

Titia de Lange

RELATED STORY: Titia de Lange: The Complex Puzzle of Chromosome Ends

Titia de Lange earned a Ph.D. in biochemistry at the University of Amsterdam and the Netherlands Cancer Institute, and did postdoctoral research with Harold Varmus at the University of California, San Francisco. She joined Rockefeller in 1990 to head the Laboratory of Cell Biology and Genetics. De Lange was appointed a professor in 1997 and the Leon Hess Professor in 1999. Today she also directs the Anderson Center for Cancer Research.

In 2013, de Lange was one of the inaugural recipients of the Breakthrough Prize in Life Sciences, and the following year she received the Canada Gairdner International Award. Her many other honors include the Vilcek Prize in Biomedical Science and the Dr. H. P. Heineken Prize. De Lange has been elected a foreign associate of the U.S. National Academy of Sciences and is a member of the Institute of Medicine, the American Academy of Arts and Sciences, the European Molecular Biology Organization and the two Dutch Royal Academies.

De Lange’s research focuses on telomeres, the elements that protect the ends of chromosomes. Her laboratory was instrumental in the discovery of shelterin, the protein complex that binds to telomeres and prevents DNA damage signaling and inappropriate DNA damage repair at chromosome ends. In collaboration with Jack Griffith, and later working with Xiaowei Zhuang, de Lange’s group showed that shelterin protects chromosome ends by remodeling telomeres into a looped structure, the t-loop, that hides the chromosome end. De Lange is also studying how the loss of telomeric DNA contributes to the development of cancer.
Bruce A. Edgar
German Cancer Research Center (Fred Hutchinson Cancer Research Center)

1993

Jun Liu +
Johns Hopkins University School of Medicine (Massachusetts Institute of Technology)

Jun Liu

Jun Liu received his undergraduate degree in chemistry from Nanjing University in Nanjing, China. He earned his M.S. in organic chemistry from The Ohio State University and his Ph.D. in biochemistry from the Massachusetts Institute of Technology. He was a postdoctoral fellow in the Department of Chemistry at Harvard University and a research associate at the National Institutes of Health. In 1993 he joined the faculty of MIT, and in 2001 he became a professor at Johns Hopkins University School of Medicine, where he directs the Pharmacology Graduate Program and the Johns Hopkins Drug Library. Liu also codirects the Cancer Chemical and Structural Biology Program of the Sidney Kimmel Comprehensive Cancer Center. His work has been recognized with a National Institutes of Health Director’s Pioneer Award and a Prostate Cancer Foundation Challenge Award. Liu is a fellow of the American Academy of Microbiology and the American Association for the Advancement of Science.

Liu’s primary research interest lies at the interface between chemistry, biology and medicine. His research group designs and synthesizes libraries of structurally novel small molecules for screening. They employ high-throughput screening to identify modulators of various cellular processes and pathways that have been implicated in human diseases, from cancer to autoimmune diseases. Once biologically active inhibitors are identified, they may serve both as probes of the biological processes of interest and as leads for the development of new drugs for treating human diseases. Among the biological processes of interest are cancer cell growth and apoptosis, angiogenesis, calcium-dependent signaling pathways, and eukaryotic transcription and translation.

Liu and his colleagues have assembled one of the largest libraries of known drugs, the Johns Hopkins Drug Library, and screened it for novel pharmacological activities for treating new diseases. They have identified several hits, the most advanced of which have entered phase 2 human clinical trials for treating a variety of human cancers. They have also identified a number of small-molecule inhibitors that target eukaryotic transcription and translation as potential anticancer drug leads. Most recently, they developed a novel macrocyle library mimicking the structural features of the immunosuppressive and anticancer drugs rapamycin and FK506, called rapafucins. They have identified a number of rapafucins targeting various cellular proteins implicated in different human diseases.
Stephen L. Mayo
California Institute of Technology
Christopher A. Walsh +
Harvard Medical School

Christopher A. Walsh

RELATED STORY: Rita Allen Foundation Scholar Christopher Walsh Receives Perl-UNC Neuroscience Prize

1991

Elizabeth A. Komives
University of California, San Diego
Jeffrey D. Macklis +
Harvard Medical School

Jeffrey D. Macklis

RELATED STORIES: Jeffrey Macklis: Making and Mending the Brain’s Machinery; Foundation Scholars Earn NIH Awards for High-Risk, High-Reward Research

Jeffrey Macklis received an S.B. in bioelectrical engineering and an S.B. in literature from the Massachusetts Institute of Technology, and completed his medical training at MIT within the Harvard/MIT Health Sciences and Technology Program. He conducted graduate and postdoctoral research with Richard Sidman at Harvard Medical School, where he also trained clinically in internal medicine at Brigham and Women’s Hospital and in adult neurology in the Harvard Neurological Training Program. Until he moved his laboratory to Massachusetts General Hospital in 2002 to direct the thematic MGH-HMS Center for Nervous System Repair, Macklis was in the Division of Neuroscience at Children’s Hospital and was codirector of the Parkinson’s Disease and Related Disorders Program at Brigham and Women’s Hospital. He assumed his current position in 2007. Macklis is the recipient of a number of awards and honors, including a Director’s Innovation Award from the National Institutes of Health, a CNS Foundation Award and a Cajal-Krieg Cortical Discoverer Prize. He is an Allen Distinguished Investigator of the Paul G. Allen Family Foundation.

Macklis’ laboratory is directed toward both 1) understanding molecular controls and mechanisms over neuron subtype specification, development, diversity, axon guidance-circuit formation and degeneration in the cerebral cortex and 2) applying developmental controls toward both brain and spinal cord regeneration and directed differentiation for in vitro therapeutic and mechanistic screening. The lab focuses on neocortical projection neuron development and subtype specification; neural progenitor/“stem cell” biology; induction of adult neurogenesis (the birth of new neurons); subtype-specific axonal growth cone biology; and directed neuronal subtype differentiation via molecular manipulation of neural progenitors and pluripotent cells. The same biology informs understanding of neuronal subtype specificity of vulnerability of human neurodegenerative and developmental diseases, in particular ALS/motor neuron disease, HSPs, PLS, Huntington’s disease, autism spectrum disorders, and Rett syndrome and ACC in particular of ASDs.
David O. Morgan
University of California, San Francisco

1990

Peter S. Kim +
Stanford University School of Medicine (Massachusetts Institute of Technology)

Peter S. Kim

RELATED STORY: Peter Kim: Sizing Up Structures and Subverting Disease

Peter Kim earned his A.B. in chemistry from Cornell University and his Ph.D. in biochemistry from the Stanford University School of Medicine. He was a Fellow at the Whitehead Institute for Biomedical Research, and joined the faculty at the Massachusetts Institute of Technology. From 2003 to 2013, he served as president of Merck Research Laboratories. In 2014, he joined the faculty at Stanford Medicine, where he also serves as a member of Stanford Bio-X, an interdisciplinary research effort; a member of the Child Research Institute; a faculty fellow of Stanford ChEM-H (Chemistry, Engineering & Medicine for Human Health); and a member of the Stanford Neurosciences Institute. He is a fellow of numerous professional organizations and a member of the Presidents’ Circle of the National Academies. He also serves on several boards, including the Medical Advisory Board of the Howard Hughes Medical Institute and the Council of the National Academy of Sciences.

Kim is studying the mechanism of viral membrane fusion and its inhibition by drugs and antibodies. His lab uses the HIV envelope protein (gp120/gp41) as a model system. Some of their studies are aimed at creating an HIV vaccine that elicits antibodies against a transient, but vulnerable, intermediate in the membrane-fusion process, called the pre-hairpin intermediate. They are also interested in protein surfaces that are referred to as “non-druggable.” These surfaces are defined empirically based on failure to identify small, drug-like molecules that bind to them with high affinity and specificity. Some of their efforts are aimed at characterizing select non-druggable targets. They are also developing methods to identify ligands for non-druggable protein surfaces.
Greg Lemke +
Salk Institute for Biological Studies

Greg Lemke

Greg Lemke received a bachelor’s degree from the Massachusetts Institute of Technology and a Ph.D. from the California Institute of Technology, where he worked with Jeremy Brockes. He conducted postdoctoral research in Richard Axel’s laboratory at the Columbia University College of Physicians and Surgeons. He joined the faculty at the Salk Institute for Biological Studies in 1985. In addition to the Rita Allen Foundation award, Lemke has received a Pew Scholars Award, a Basil O’Connor Starter Scholar Award from the March of Dimes and a Javits Neuroscience Investigator (Merit) Award from the National Institutes of Health. He served as editor-in-chief of Molecular and Cellular Neuroscience from 1995 to 2005. He is a fellow of the American Association for the Advancement of Science.

The Lemke laboratory has made significant contributions to understanding intercellular communication, specifically with respect to the role that receptor tyrosine kinases (RTKs) play in embryonic development and adult physiology. The lab first identified 11 of the 58 RTKs encoded in mammalian genomes, discovering the TAM and DDR RTK families, as well as new members of the ErbB, FGF and Eph families. Together with collaborators, they identified the ligands that activate DDR and TAM receptors. The Lemke group’s generation and analysis of mouse mutants for ErbB4, a receptor for neuregulin-1 (a ligand that Lemke puried as a graduate student at Caltech), revealed essential roles for neuregulin/ErbB signaling in cardiac myocyte morphogenesis and nervous system development. Their systematic genetic alteration of EphA receptor gradients in the retina provided a definitive genetic test of the role that these gradients play in the topographic wiring of neuronal connections during brain development. They formulated and then tested a quantitative theory for this gradient-driven process. Their most influential contributions derive from the study of the TAM receptors and their ligands.
Marilyn D. Resh
Memorial Sloan Kettering Cancer Center (Princeton University)

1989

Andrew Z. Fire +
Stanford University School of Medicine (Carnegie Institution of Washington)

Andrew Z. Fire

Andrew Fire received a B.A. in mathematics from the University of California, Berkeley, and a Ph.D. from the Massachusetts Institute of Technology. He conducted postdoctoral research at the Medical Research Council Laboratory in Cambridge, England. From 1986 to 2003, Fire was on the staff of the Carnegie Institution of Washington’s Department of Embryology in Baltimore, Maryland. During his time in Baltimore, he also assumed the position of Adjunct Professor of Biology at Johns Hopkins University. In 2003, he joined the faculty of the Stanford University School of Medicine. Fire was awarded the Nobel Prize in Physiology or Medicine in 2006 along with Craig Mello “for their discovery of RNA interference—gene silencing by double-stranded RNA.”

The Fire lab studies the mechanisms by which cells and organisms respond to genetic change. The genetic landscape faced by a living cell is constantly changing. Developmental transitions, environmental shifts and pathogenic invasions lend a dynamic character to both the genome and its activity pattern. Fire’s group explores a variety of natural mechanisms that are utilized by cells adapting to genetic change. These include mechanisms activated during normal development and systems for detecting and responding to foreign or unwanted genetic activity. At the root of these studies are questions of how a cell can distinguish “self ” versus “nonself ” and “wanted” versus “unwanted” gene expression.
Nouria Hernandez +
University of Lausanne (Cold Spring Harbor Laboratory)

Nouria Hernandez

Nouria Hernandez obtained a master’s degree from the University of Geneva and a Ph.D. in molecular biology from the University of Heidelberg. She did postdoctoral research with Alan Weiner at Yale University, and in 1987 she joined Cold Spring Harbor Laboratory. In 1999 she became an Investigator of the Howard Hughes Medical Institute. In 2005 she joined the faculty of the University of Lausanne in Switzerland. In August 2016 she will become Rector of the University of Lausanne. Hernandez is a member of the European Molecular Biology Organization and a recipient of the Cloëtta Prize from the Professor Dr Max Cloëtta Foundation.

Hernandez’s research focuses on mechanisms of gene regulation in mammals. RNA polymerase III (Pol III) synthesizes a number of RNA products involved in protein translation, maturation of other RNA molecules and other processes. The Hernandez lab aims to understand how Pol III genes are regulated and the consequences of deregulated Pol III transcription. Pol III is tightly controlled in response to environmental cues, yet in mammalian cells, a genome-scale picture of Pol III regulation and the role played by the Pol III repressor MAF1 is lacking. Such fundamental questions as whether Pol III genes are regulated globally or individually, and whether MAF1 binds to Pol III genes under adverse conditions (and to which genes), have remained either unanswered or only poorly explored. Hernandez’s group has recently shown that the regulation of Pol III genes is not a uniform process affecting all genes similarly; rather, groups of Pol III genes are differentially regulated. Pol III recruitment and transcription are tightly linked to MAF1, which selectively localizes to Pol III-occupied loci, even under serum-replete conditions, and increasingly targets transcribing Pol III in response to serum starvation. A Maf1 knockout mouse displays several lipid metabolism abnormalities, an observation that links Pol III transcription to lipid metabolism.
Ronald D. Vale +
University of California, San Francisco

Ronald D. Vale

RELATED STORY: Moving Science Forward: Ron Vale Shares the Marvels of Cellular Motion, Brings Biology to New Audiences

1988

Gilbert Chu +
Stanford University School of Medicine

Gilbert Chu

RELATED STORY: Gilbert Chu: DNA Dreamer

Gilbert Chu received a B.A. in physics from Princeton University, a Ph.D. in theoretical physics from the Massachusetts Institute of Technology, and an M.D. from Harvard Medical School. His laboratory focuses on DNA repair, having identified a protein involved in repair of bulky DNA adducts and a protein involved in repair of DNA double-strand breaks. He identified the role of ammonia in “chemobrain,” co-invented a device for measuring blood ammonia, and cares for cancer patients. He has patents for: a device that separates megabase-sized DNA molecules; a method that analyzes genome-wide expression profiles; a gene expression signature that predicts toxicity from radiation therapy; and a protein complex that joins mismatched DNA ends. In addition to a Rita Allen Foundation award, Chu has received a Burroughs-Wellcome Clinical Scientist Award, three Kaiser Awards for Excellence in Preclinical Teaching, and a Lawrence H. Mathers Award for Exceptional Commitment to Teaching and Active Involvement in Medical Student Education.

To understand how human cells repair damaged DNA, the Chu laboratory has focused on nucleotide excision repair and non-homologous end joining (NHEJ). Their current focus is the molecular mechanism for NHEJ, which repairs DNA double-strand breaks induced by ionizing radiation or generated during V(D)J recombination.

To understand how human cells respond to DNA damage, Chu’s group invented methods for analyzing gene expression profiles. These methods include Significance Analysis of Microarrays and Prediction Analysis of Microarrays. They used the methods to define transcriptional responses to ultraviolet radiation and ionizing radiation, and to identify a set of gene responses that predict toxicity from radiation therapy.
Stephen L. Hauser
University of California, San Francisco
Jon D. Levine +
University of California, San Francisco

Jon D. Levine

RELATED STORY: Jon Levine: A Passion for Deciphering Pain

Jon Levine received a B.S. in biophysics and an M.S. in bioengineering from the University of Michigan, and earned a Ph.D. in neurobiology at Yale University, where he worked with Robert Wyman. He conducted postdoctoral research on Drosophila neurogenetics in Donald Kennedy’s laboratory at Stanford University. Levine completed his medical training at the University of California, San Francisco, where he was also a fellow in rheumatology and clinical pharmacology. He joined the faculty of UCSF in 1983. In addition to a Rita Allen Foundation award, Levine has received a Chancellor’s Commendation for Research Excellence from the University of California, a Hartford Foundation fellowship, and a Frederick W.L. Kerr Basic Science Research Award from the American Pain Society.

Levine’s laboratory employs a multidisciplinary approach of molecular, biochemical, in vitro and in vivo electrophysiological and behavioral techniques to evaluate mechanisms underlying pain and analgesia. His team is investigating signal transduction mechanisms for mechanical, thermal and chemical stimulus-induced activation of sensory neurons and mechanisms underlying sensitization of responses to these stimuli. They have described a novel transducer mechanism for mechanical stimuli, as well as second messenger pathways mediating nociceptor sensitization in inflammatory and neuropathic pain. They are investigating the modulation of transduction by opioids, including the mechanisms underlying opioid tolerance and dependence. Levine’s group also studies central nervous system circuits that mediate analgesia, and has described a novel analgesia circuit involving limbic pathways, as well as sexual dimorphism in pain and analgesic mechanisms. Finally, they are investigating neural and endocrine (stress axis) contributions to inflammation and the immune response. Their work has elucidated a physiological mechanism consisting of a negative feedback inhibition of the inflammatory response, involving neural and endocrine mechanisms.

1986

Adrienne A. Brian
University of California, San Diego
Charles D. Gilbert +
The Rockefeller University

Charles D. Gilbert

Charles Gilbert received his M.D. and Ph.D. from Harvard Medical School, where he held an academic appointment until he joined The Rockefeller University in 1983. A member of the National Academy of Sciences and the American Academy of Arts and Sciences, he has received numerous awards, including the W. Alden Spencer Award from the Columbia University College of Physicians and Surgeons and the Edward M. Scolnick Prize in Neuroscience from the McGovern Institute for Brain Research at MIT. He is a member of the Rita Allen Foundation’s Scientific Advisory Committee.

Gilbert’s work focuses on the brain mechanisms of visual perception and learning. He studies the way in which the brain analyzes visual images, and how this analysis is shaped by experience and by higher-order cognitive influences. A major focus of his work is on plasticity of the visual cortex: the way in which cortical circuitry and function change during normal perceptual learning and during functional recovery following lesions of the central nervous system. He investigates the mechanisms of information processing by the brain at the molecular, circuit and perceptual levels. He has revealed its dynamic nature, showing the influence of attention, expectation and perceptual task on cortical function.
Ronald D.G. McKay
Johns Hopkins University School of Medicine (Massachusetts Institute of Technology)

1985

Bruce P. Bean
Harvard Medical School
Brent H. Cochran
Tufts University School of Medicine (Massachusetts Institute of Technology)
Stanley M. Goldin +
Harvard Medical School

Stanley M. Goldin

Stanley Goldin earned undergraduate and master’s degrees in chemical engineering from the Massachusetts Institute of Technology, and a Ph.D. from Harvard University. He has served on the Harvard Medical School faculty since 1979. Formerly an associate professor and the director of Harvard’s Pharmacological Sciences Training Program, he is now on faculty of the National Science Foundation-funded Cognitive Rhythms Collaborative, an inter-institutional research collaborative devoted to elucidating brain mechanisms, spawning new therapies for brain disorders.

Goldin is a senior inventor on 25 U.S. biotechnology patents; his laboratory originated award-winning research techniques and devices that have been fruitfully employed to elucidate molecular mechanisms underlying brain waves and brain oscillation circuitry—processes now known to play an important role in long-term brain changes (neuroplasticity) and memory formation. As a scientific cofounder of the biotechnology company Cambridge NeuroScience, he also led research producing a novel neuroprotective compound reaching advanced clinical trials for stroke and traumatic brain injury. His honors include a McKnight scholarship, a Sloan Research Fellowship, a Searle Scholars Award, and the Clapp and Poliak Award for Engineering Design. Goldin is now finishing a book, Ascent of the Human Brain, on modern neuroscience’s impact on our understanding of human consciousness and evolution.
Winship Herr +
University of Lausanne (Cold Spring Harbor Laboratory)

Winship Herr

Winship Herr obtained his B.A. from the University of California, Santa Cruz, and a Ph.D. in biochemistry and molecular biology from Harvard University, where he worked with Walter Gilbert. Following six months in the laboratory of Frederick Sanger at the MRC Laboratory of Molecular Biology in Cambridge, England, Herr joined Cold Spring Harbor Laboratory as a postdoctoral fellow in 1983. He was appointed to the laboratory staff in 1984, and remained until 2005, when he joined the University of Lausanne. In 1998, Herr spearheaded the establishment of the Watson School of Biological Sciences and the accreditation of CSHL as a Ph.D. degree-granting institution. He served as the school’s founding dean from 1998 to 2004. Besides being a Rita Allen Foundation Scholar, Herr is a former National Science Foundation predoctoral fellow, Helen Hay Whitney postdoctoral fellow and CSHL Lita Annenberg Hazen Professor of Biological Sciences. He is a member of the European Molecular Biology Organization and has received an honorary Doctor of Science degree from the Watson School of Biological Sciences.

Herr is interested in how the two complete sets of instructions contained within the genomes we inherit from our parents direct a single cell—the zygote—to become an adult human being. This process results from controlled patterns of gene expression that are maintained, as well as changed, during many rounds of cell division, differentiation and death. Control of gene transcription is fundamental to these processes—with genetic and epigenetic defects in transcriptional regulation often leading to human diseases, including cancer. To investigate transcriptional regulation, Herr’s laboratory studies HCF-1, a key regulator of human cell proliferation. Within our cells, HCF-1 resides at many transcriptional start sites, recognizing promoter-specific transcription factors and recruiting enzyme complexes involved in chromatin structure regulation (e.g., states of histone acetylation and methylation) for activation and repression of transcription.
Carl S. Parker +
California Institute of Technology

Carl S. Parker

Carl Parker earned his B.A. from the University of Rochester and his Ph.D. from Washington University in St. Louis. He joined the faculty at Caltech in 1981.

Research in the Parker lab focuses on the molecular mechanisms cells use to respond to physiological stress such as heat shock. He and his collaborators are interested in understanding how heat, for example, is transduced into a massive transcriptional activation response that results in the synthesis of heat shock proteins.

1984

Thomas M. Jessell +
Columbia University Medical Center (Harvard Medical School)

Thomas M. Jessell

RELATED STORY: Thomas Jessell: Linking Molecules to Perception and Motion

Thomas Jessell earned his B.Pharm. from the University of London and his Ph.D. in neuropharmacology from the University of Cambridge, where he worked with Leslie Iverson. Their collaboration led to the finding that opiate drugs inhibit the release of substance P from the terminals of primary sensory nerve cells that mediate nociception [the sensing of potentially harmful stimuli]. He completed postdoctoral work at Harvard Medical School with Gerald Fischbach (now the Scientific Director of e Simons Foundation), and joined the Harvard Department of Neurobiology faculty in 1981. He moved to Columbia University in 1985, where he codirects both the Kavli Institute for Brain Science and the Mortimer B. Zuckerman Mind Brain Behavior Institute. He is also an Investigator of the Howard Hughes Medical Institute.

Jessell served on the Rita Allen Foundation’s Scientific Advisory Committee from 1999 to 2007. He is a Fellow of the Royal Society of London and a Foreign Associate of the U.S. National Academy of Sciences. He was a co-recipient of the 2008 Kavli Prize in Neuroscience and a recipient of the 2012 Canada Gairdner International Award.

Jessell’s research focuses on the developmental assembly of the vertebrate central nervous system. He has defined the general logic, as well as many of the key cellular and molecular mechanisms, that control the assembly and functional organization of circuits in the spinal cord. His research has revolutionized our understanding of neural development and laid the foundation for a better understanding of the cellular physiology of the spinal cord and reflex behavior.
Carl F. Nathan +
Weill Cornell Medical College (The Rockefeller University)

Carl F. Nathan

Carl Nathan is R.A. Rees Pritchett Professor and Chair of the Department of Microbiology and Immunology at Weill Cornell Medical College. He co-chairs the Program in Immunology and Microbial Pathogenesis at Weill Cornell Graduate School of Medical Sciences. A graduate of Harvard College and Harvard Medical School, he trained in internal medicine and oncology at Massachusetts General Hospital, the National Cancer Institute and Yale before joining the faculty of The Rockefeller University. Nathan is a member of the National Academy of Sciences, the National Academy of Medicine and the American Academy of Arts and Sciences. He is the 2009 recipient of the Robert Koch Award for his research on mechanisms of defense against bacterial pathogens and the 2013 recipient of the Anthony Cerami Award in Translational Medicine.
H. Earl Ruley
Vanderbilt University School of Medicine (Massachusetts Institute of Technology)

1979

John Condeelis
Albert Einstein College of Medicine
Paul H. Patterson +
California Institute of Technology (Harvard Medical School)

Paul H. Patterson

Paul Patterson (1943–2014) completed his undergraduate studies at Grinnell College. He earned a Ph.D. from Johns Hopkins University, where he worked with William Lennarz. As a postdoc at Harvard Medical School, Patterson conducted pioneering research on neural plasticity with Edwin Furshpan and David Potter. He then became a faculty member at Harvard, before moving to Caltech in 1983. Patterson explored links between the immune system and the nervous system—he became known as a “neuroimmunologist”—and developed mouse models of schizophrenia and autism. He was a fellow of the American Association for the Advancement of Science.
Stephen A. Udem +
Albert Einstein College of Medicine

Stephen A. Udem

Stephen Udem (1994–2014) studied chemistry at City College, and earned M.D. and Ph.D. degrees in the Medical Scientist Training Program at Albert Einstein College of Medicine. He worked as an infectious disease clinician at several New York and New Jersey hospitals over the course of his career. Udem also made critical contributions to the fields of virology and vaccinology, first through academic research and later through his work in vaccine development in both industry and nonprofit settings.

Much of his research focused on mechanisms of viral persistence in the central nervous system. From 1994 to 2006, he held various leadership positions at Wyeth, where he managed the expansion of the company’s vaccine programs. Udem then directed vaccine development efforts at the International AIDS Vaccine Initiative before establishing his own consultancy practice for vaccine R&D. He was a member of the American Medical Association and the American Association for the Advancement of Science.

1978

Kathleen M. Foley +
Memorial Sloan Kettering Cancer Center (Cornell University Medical College)

Kathleen M. Foley

RELATED STORY: Pioneering Pain Researcher Invests in Next Generation of Scholars

Kathleen Foley is recognized as a leader in developing global standards for pain management and palliative care. She earned her B.S. from St. John’s University and her M.D. from Cornell University Medical College. She completed residencies at Memorial Sloan Kettering Cancer Center and Cornell, and was a special fellow in neuro-oncology at MSKCC. In the 1980s, she served as Chief of Memorial Sloan Kettering’s Pain and Palliative Care Service, which she helped to establish. This first-of-its kind, team-based service ensures that pain management and palliative care are integrated into cancer treatment for all patients. From 1994 to 2003, she directed the Project on Death in America, which focused on changing attitudes and policies toward end-of-life care. She also served as director of the World Health Organization’s Collaborating Center for Cancer Pain Research and Education at Memorial Sloan Kettering.

Foley joined the Rita Allen Foundation’s Scientific Advisory Committee in 1997 and became the Medical Advisor in 2009, leading the committee in selecting each class of Scholars. She introduced the idea of a partnership between the Rita Allen Foundation and the American Pain Society to identify and support promising young investigators working in this field. Each year since 2009, two Rita Allen Foundation Scholars have been designated as recipients of the Award in Pain.

Foley has received numerous awards, including the Medal of Honor from the American Cancer Society, the David Karnovsky Award from the American Society of Clinical Oncology and the Frank Netter Award of the American Academy of Neurology.
William W. Hall
University College Dublin (The Rockefeller University)
Thomas P. Maniatis +
Columbia University Medical Center (California Institute of Technology)

Thomas P. Maniatis

RELATED STORY: Tom Maniatis: Mastering Methods and Exploring Molecular Mechanisms
Graham C. Walker +
Massachusetts Institute of Technology

Graham C. Walker

Graham Walker received his Honors B.Sc. from Carleton University in Ottawa, Ontario, and his Ph.D. from the University of Illinois at Urbana-Champaign. He conducted postdoctoral research at the University of California, Berkeley, and joined MIT’s biology department in 1976. He is an affiliate member of MIT’s Koch Institute of Integrative Cancer Research. Walker was elected to the National Academy of Sciences in 2013 and is an American Cancer Society Professor and Howard Hughes Medical Institute Professor. He is a fellow of the American Academy of Arts and Sciences, the American Association for the Advancement of Science and the American Academy of Microbiology. He has also received other awards, including an Environmental Mutagen Society Award, a John Simon Guggenheim Memorial Fellowship and a Woodrow Wilson Fellowship. Walker is a MacVicar Faculty Fellow for his undergraduate teaching. Walker was editor and then editor-in-chief of the Journal of Bacteriology for 16 years, and coauthored DNA Repair and Mutagenesis (ASM Press).

Walker has contributed to our understanding of how cells respond to damage to their DNA and the mechanisms they use to repair or tolerate such DNA damage. His lab provided the first direct evidence, in any organism, that physiological responses to DNA damage can be caused by changes in transcription, and that the induced genes encode functions required for DNA repair, mutagenesis and cell cycle checkpoints. Walker was the first to clone and characterize genes encoding translesion synthesis (TLS) DNA polymerases and key mismatch repair proteins. Walker’s recent work has demonstrated that interfering with the function of mammalian error-prone TLS DNA polymerases can aid chemotherapy and has unexpectedly provided insights into the action of bactericidal antibiotics. Walker’s studies of the symbiosis between the nitrogen-fixing bacterium Sinorhizobium meliloti and legumes have provided detailed insights into the molecular mechanisms necessary for the bacteria to establish the chronic infection that underlies the symbiosis. They have also led to the discovery of relationships between rhizobia and chronic intracellular human pathogens and the discovery of the missing step in vitamin B12 biosynthesis. Walker used his HHMI Professorship to run an education group that developed the internationally used, freely available educational software StarBiochem, StarGenetics and StarCellBio.

1976

James B. Lewis
Foresight Institute (Cold Spring Harbor Laboratory)
Robert A. Weinberg +
Massachusetts Institute of Technology

Robert A. Weinberg

RELATED STORIES: Robert Weinberg: The Genesis of Cancer Genetics, Rita Allen Foundation Scholar Robert Weinberg Awarded Salk Institute Medal for Research Excellence

An internationally recognized authority on the genetic basis of human cancer, Robert Weinberg is a founding member of the Whitehead Institute for Biomedical Research and the first Director of the Ludwig Cancer Center at the Massachusetts Institute of Technology. Over the past three decades, he has made breakthrough discoveries in the molecular and genetic roots of cancers. His lab discovered the first oncogene in 1982 and the first tumor suppressor gene in 1986. Most recently, Weinberg and his colleagues were the first to define the genetic rules that must be followed in order for a normal human cell to be transformed into a human cancer cell. The author or editor of six books and more than 420 articles, Weinberg is well known for his comprehensive cancer textbook, The Biology of Cancer. He is an elected member of the National Academy of Sciences and a fellow of the American Academy of Arts and Sciences. He is also a member of the American Philosophical Society and the National Academy of Medicine. He has received the National Medal of Science (1997), the Wolf Prize in Medicine (2007), the Otto Warburg Medal (2007) and the Breakthrough Prize in Life Sciences (2013).

Weinberg’s lab is primarily concerned with how oncogenes, their normal counterparts (proto-oncogenes) and tumor suppressor genes fit together in the complex circuitry that controls cell growth. His lab recently succeeded in creating the first genetically defined human cancer cells. He is particularly interested in applying this knowledge to improve the diagnosis and treatment of breast cancer. At present his lab seeks to understand how a malicious population of tumor cells, called cancer stem cells, develop their metastatic powers, and what biological conditions are required to eliminate them.
Harold M. Weintraub +
Fred Hutchinson Cancer Research Center (Princeton University)

Harold M. Weintraub

Harold Weintraub (1945–1995) earned a bachelor’s degree from Harvard College and an M.D.-Ph.D. from the University of Pennsylvania. He conducted postdoctoral research with Sydney Brenner and Francis Crick at the Medical Research Council in Cambridge, England, before joining the faculty of Princeton University. Weintraub moved to the Fred Hutchinson Cancer Research Center in Seattle in 1978. He is best known for the discovery of the myoD gene, which encodes a master regulator of muscle cell differentiation. He was a member of the National Academy of Sciences and was a Howard Hughes Medical Institute Investigator from 1990 to 1995.

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