- Rita Allen Foundation

All Scholars

Since 1976, the Rita Allen Foundation has awarded millions of dollars in grants to early-career biomedical scholars. These grants allow Rita Allen Foundation Scholars to establish labs and pursue research directions with above-average risk and promise. See below for a full list of Scholars, or read more about the Rita Allen Foundation Scholars program.

2011

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

Briana Burton

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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

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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

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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

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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.

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