- 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.

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.

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