University of Sussex, England
Appointed in 1983
Control of mitosis in fission yeast
University of California, San Diego
Appointed in 1984
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University of California, San Diego
Appointed in 1984
Developmental regulation of neuroendocrine gene expression
Weizmann Institute of Science, Israel
Appointed in 1973
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Weizmann Institute of Science, Israel
Appointed in 1973
Fiber fractionation
Massachusetts General Hospital
Appointed in 2001
Comparative genomics and neuronal differentiation
Harvard University Medical School
Appointed in 2020
Novel roles of ultraconserved elements in genome integrity
Ultraconserved elements (UCEs) are a set of DNA sequences that exhibit perfect conservation across the genomes. I learned of UCEs and their putative role in maintaining genome integrity at a seminar by Dr. Chao-ting Wu. Scattered across genomes, unique, and 200bps or greater in length, UCEs have remained unchanged for over 300 million years. Yet, their extreme sequence conservation is still a mystery. Although my Ph.D. training is in the DNA repair field, I decided to join Dr. Chao-ting’s lab as a postdoctoral researcher and explore the biology of UCEs. Previous studies have demonstrated that UCEs can contain transcription factor binding motifs an function as enhancers to regulate tissue-specific transcription. However, no regulatory or proteincoding functions can explain such extreme sequence conservation. My research will focus on testing a model that can explicitly address such an explanation. I hypothesize that homologous UCEs compare their sequences via pairing and any detected discrepancies in sequence or copy number will lead to cell death and/or disease onset. As a result, genome integrity would be maintained by culling out cells carrying deleterious rearrangements. I will assay this model with different approaches Рa) computational analyses, b) CRISPR-based genome editing, and c) imaging techniques. Ultimately, the potential of UCEs to sense and cull deleterious rearrangements genome-wide offers a unique yet intriguing and still largely unexplored potential general strategy for treating diseases derived from rearrangements, regardless of the etiology of diseases.
Stanford University
Appointed in 2004
New York University
Appointed in 2001
Washington University in St. Louis
Appointed in 2025
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Washington University in St. Louis
Appointed in 2025
The functional role of transposable element-derived transcripts in cancer progression
Dr. Wesley Saintilnord is interested in how transposable elements (TEs), DNA sequences that can move from one location in a genome to another, can exploit epigenetic pathways that then lead to their aberrant reactivation in cancer cells to rewire gene expression programs. In his fellowship, Saintilnord will examine how TEs functionally contribute to cancer progression.
Saintilnord developed his expertise in epigenetic mechanisms during his Ph.D. research at the University of Kentucky in Dr. Yvonne Fondufe-Mittendorf’s lab now at the Van Andel Institute. In his first project, Saintilnord showed that cadmium exposure changes how many genes are turned on during sperm development by affecting DNA methylation. In another study, he found that certain cancer-associated variants of a histone protein make DNA wrap more tightly, changing how genes are expressed. Collectively, his research demonstrates how environmental exposure, and oncogenic mutations rewire gene expression through epigenetic pathways.
Now, in Dr. Ting Wang’s lab at Washington University in St. Louis, he will dissect why cancer cells take control of TEs for gene regulation and how TE-generated transcripts drive tumorigenesis. He will develop a high-throughput screen to evaluate tumor-enriched TE transcripts in classical cancer phenotypes. Then, Saintilnord will evaluate which of these transcripts encode functional proteins that modulate cell signaling and chromatin dynamics. Saintilnord’s studies will provide fundamental insights into TE biology in cancer cells and may reveal novel therapeutic strategies to combat TE-mediated oncogenic programs.
National Institutes of Health
Appointed in 1956
Biosynthesis of gramicidin S in bacteria
Massachusetts General Hospital
Appointed in 1995
A system to identify novel mammalian regulators
Stanford University
Appointed in 1995
H pylori genes expressed in gastric mucosa infection
New York University
Appointed in 1966
RNA code
Harvard University
Appointed in 1991
Kinetics of protein folding
Instituto Superiore di Sanita, Italy /
Universite de Paris, France
Appointed in 1957
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Instituto Superiore di Sanita, Italy / Universite de Paris, France
Appointed in 1957
Carbohydrate metabolism
Scripps Research Institute
Appointed in 1999
Directed evolution of a site-specific recombinase
Scripps Research Institute
Appointed in 2018
Molecular structure and mechanism of Piezo mechanotransduction channels
Piezo proteins are ion channels that sense mechanical force in various physiological pathways, including touch sensation, breathing, and vascular development. Mutations in Piezo cause diseases associated with mechanotransduction defects, including distal arthrogryposis and dehydrated hereditary stomatocytosis. Piezos are unrelated to other known ion channels, and how they transduce mechanical force into channel opening remains unknown. As a joint postdoc in Andrew Ward and Ardem Patapoutian labs, I use cryo-electron microscopy and other biophysical approaches to gain a mechanistic understanding of Piezo function.”
University of Utah
Appointed in 1982
Human polymorphisms due to genomic rearrangements
University of Oregon
Appointed in 1981
National Institutes of Health
Appointed in 1981
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National Institutes of Health
Appointed in 1981
Regulation of mRNA in embryonic Xenopus
University of Utah
Appointed in 2013
ESCRT-III mediated membrane scission
Computational modeling will be coupled with experiment to investigate the mechanism by which Endosomal Sorting Complexes Required for Transport (ESCRT)-III complexes remodel and sever membranes. The ESCRT pathway relates to cancer pathogenesis by: mediating downregulation of membrane-bound receptors; catalyzing the abscission stage of cytokinesis; and controlling exosome formation. Of the five essential core ESCRT complexes, the ESCRT-III complex uniquely encodes the membrane severing activity. ESCRT-III subunits form filaments that can bind membranes, selforganize into higher-order assemblies, and use these assemblies to constrict membranes and promote fission. Newly emerging cryo-EM reconstructions of ESCRT-III assemblies make it possible to create the first models of these systems that incorporate discrete subunit structures. Using these models, we will investigate: how these filaments form rings with different diameters; how membrane interactions and curvature affect filament structure; and how lateral interactions between adjacent filaments accommodate changes in curvature. Experimental measurements of the physical properties of wild type and mutant ESCRT-III filaments will be used to validate these models and test their predictive power. This integration of experiment and theory should identify, at a fundamental level, properties driving ESCRT-III-mediated membrane remodeling and fission.
Rockefeller University
Appointed in 1974
Messenger RNA
Rockefeller University
Appointed in 1975
Genetics of avian RNA tumor viruses
University of California, San Francisco
Appointed in 1995
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University of California, San Francisco
Appointed in 1995
Thymidylate synthase and structure-based drug design
University of Oxford, England
Appointed in 1987
Isolation and characterization of fission yeast cell division cycle mutant
Yale University
Appointed in 1977
Gene transfer
Princeton University
Appointed in 1984
Physical aspects of adenovirus (AD) which affect AD gene expression
University of Frankfurt, Germany
Appointed in 1968
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University of Frankfurt, Germany
Appointed in 1968
Amino acid transport in Ehrlich ascites tumor cells
Harvard University
Appointed in 1997
Understanding the molecular basis of 8-oxo-G repair
Harvard University
Appointed in 2011
Intelligent drug delivery by dynamic nucleic acid nano-devices
Imperial Cancer Research Fund Laboratories, England
Appointed in 1974
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Imperial Cancer Research Fund Laboratories, England
Appointed in 1974
Replication of herpes virus in isolated nuclei
Stanford University
Appointed in 1981
Mechanisms of amplification of folate reductase genes
Yale University
Appointed in 1976
Neutron scattering of the E. coli ribosome
University of California, San Francisco
Appointed in 2015
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University of California, San Francisco
Appointed in 2015
Characterization of the endoplasmic reticulum membrane protein complex
Polytopic membrane proteins undergo a complicated folding process, whereby they must be co-translationally targeted to the endoplasmic reticulum (ER) for maturation and export to cellular membranes. While our understanding of the chaperones involved in soluble protein folding has rapidly expanded, there is little known about the chaperones dedicated to folding and quality control of membrane proteins. Recently, a conserved ER membrane protein complex (EMC) was discovered from a genetic screen in yeast aimed at identifying genes that disrupt the ER protein folding environment. Genetic interaction patterns arising from deletion of the EMC and preliminary biochemical data suggest the EMC may function as a chaperone for polytopic membrane proteins. As a postdoctoral fellow in the Frost and Weissman laboratories at UCSF, I plan to use a combination of approaches ranging from cryo-electron microscopy to genetics and cell biology to elucidate how the EMC affects membrane protein topology in yeast and human cells.
University of California, Berkeley
Appointed in 2008
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University of California, Berkeley
Appointed in 2008
The role of organelle-microtubule linker proteins in the spatial organization of the cell
Walter and Eliza Hall Institute of Medical Research, Australia
Appointed in 1971
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Walter and Eliza Hall Institute of Medical Research, Australia
Appointed in 1971
Messenger RNA's coding for antibody globulins
Whitehead Institute for Biomedical Research
Appointed in 2020
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Whitehead Institute for Biomedical Research
Appointed in 2020
Understanding extracellular modifiers of morphogen signaling
Animals rely on effective coordination of cell behavior in all phases of their development and lifespan. Cells communicate to coordinate their activity using several physical or chemical communication strategies, which are often interdependent. One communication strategy central in development and in adult animals relies on secreted signaling proteins that bind membrane-tethered receptors in diverse target tissues to affect cell identity or behavior. Whereas we understand in great detail how signals are synthesized, secreted, received and processed, we understand comparatively very little about how signals travel from their origin to their destination. I use molecular genetic and synthetic biology tools in cultured mammalian cells to reconstitute cell signaling events, and I use these reconstituted signaling pathways to understand how secreted protein signals navigate the extracellular environment in developing or adult tissues.
California Institute of Technology
Appointed in 1971
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California Institute of Technology
Appointed in 1971
Structure of attachment site of lambda phage n the bacterial chromosome
Princeton University
Appointed in 1997
H19: The function of a noncoding RNA
Carnegie Institute for Science
Appointed in 1991
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Carnegie Institute for Science
Appointed in 1991
Regulation of developmental arrest in oogenesis
University of California, Irvine
Appointed in 2003
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University of California, Irvine
Appointed in 2003
University of Wisconsin /
Rockefeller Institute
Appointed in 1945
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University of Wisconsin / Rockefeller Institute
Appointed in 1945
Enzymatic studies of nucleic acids
Whitehead Institute for Biomedical Research
Appointed in 2023
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Whitehead Institute for Biomedical Research
Appointed in 2023
Origin and function of macrophage heterogeneity in the tumor
Tumor-associated macrophages (TAMs) are the most abundant innate immune cell type in tumors. TAMs can either inhibit or support tumor progression, though it is unclear how their dichotomous functions are regulated. Dr. Alexandra Schnell predicts that the functional heterogeneity of TAMs may be due to distinct lineage origins and cell plasticity. To investigate these hypotheses, Dr. Schnell is developing a myeloid-specific lineage tracing tool to track TAM heterogeneity in tumors, and in response to immunotherapies. Schnell will conduct these experiments in Dr. Jonathan Weissman’s and Dr. Kipp Weiskopf’s labs at the Whitehead Institute. By better understanding TAM heterogeneity, Schnell hopes to enable the development of TAM-targeted cancer immunotherapies that specifically target tumor-promoting macrophages.
During her PhD, Schnell studied the fundamental mechanisms of the immune system in Dr. Vijay Kuchroo’s lab at Harvard Medical School. There, Dr. Schnell performed lineage tracing of immune cells during autoimmune inflammation. Her studies provided a mechanism for how homeostatic intestinal immune cells act as a reservoir for pathogenic inflammation elsewhere in the body. With this background in immunity and lineage tracing, Dr. Schnell will now investigate how the heterogeneity of tumor immune cells can be leveraged to generate new cancer immunotherapies.
Rockefeller University
Appointed in 2004
Asymmetric versus symmetric divisions in stem cells
Rockefeller University
Appointed in 1992
Characterizing the activation of YAP kinase by v-Src
Fred Hutchinson Cancer Center
Appointed in 2016
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Fred Hutchinson Cancer Center
Appointed in 2016
Do genetic conflicts shape the actin cytoskeleton in eukaryotes?
I am interested in how evolution has shaped the eukaryotic actin cytoskeleton. The actin cytoskeleton is a critical force-generating polymer that powers fundamental cellular processes, including cell motility, vesicle transport and cytokinesis. Despite actins being among the most highly conserved proteins in eukaryotes, a number of actin variants and their regulators show strong signatures of genetic innovation in Drosophilids. Birth and death of novel actins have occurred between lineages and a few actin genes appear to rapidly evolve, suggestive of positive selection. Using genetic, evolutionary and cell biological analyses, I am investigating the evolutionary causes and functional consequences of genetic changes among components of the actin cytoskeleton with Drosophila melanogaster as the model organism. Exploring the actin cytoskeleton and its regulation from an evolutionary vantage will provide insight into the selective pressure on actins and how it is harnessed in many cellular processes.
Harvard University
Appointed in 2005
Single molecule kinetics of reverse transcriptase
Yale University
Appointed in 1976
Cyclic nucleotides and synaptic transmission
Columbia University
Appointed in 2009
Development of optogenetic tools to probe the formation of social memory
I am developing methods to control gene expression and recombination with light.  This will allow greater spatial and temporal control than can be achieved with current genetic and chemical methods.
I majored in chemistry and biology at the University of Virginia, where I worked in the lab of Michael Timko. I discovered that, even though I was studying an algae that most people have never heard of, it was still really cool to be the first in the world to know something.  Also, during my first year, the UVA football team was briefly ranked in the top ten, an accomplishment which I can only assume was thanks to my presence.  In graduate school at Rockefeller University, I did my research in the laboratory of Tom Muir, playing with molecular legos for five and a half years and getting a PhD out of that experience as a bonus.  Currently I’m in Richard Axel’s lab at Columbia, where I feel a little out of place among the real biologists.  All my time outside of work is now taken up chasing around a two-year-old.
Columbia University
Appointed in 1948
Nucleic acid metabolism
University of Oxford, England
Appointed in 1968
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University of Oxford, England
Appointed in 1968
Weizmann Institute of Science, Israel
Appointed in 1986
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Weizmann Institute of Science, Israel
Appointed in 1986
Regulation of IgE production by feeR bearing lymphocytes