Directory - Jane Coffin Childs Memorial Fund

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Year Appointed

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XinXin Ge, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2021

Primary visual cortex (V1) receives visual information ascending from the eyes as well as

descending from higher order visual areas. As such, V1 is the first cortical stage of visual processing at the intersection between two major pathways, the bottom-up, feedforward and the top-down, feedback streams of visual information. Despite current advances in understanding the integration of information from feedforward and feedback pathways in V1, our knowledge relative to how single neurons in V1 combine information from different origins to form their responses to visual stimuli remains rudimentary. To investigate this question, we apply advanced volumetric imaging technique to measure populations of excitatory synaptic inputs impinging onto single neurons in V1. Using this approach, we characterize the visual response properties of excitatory synaptic inputs to visual stimuli as well as the spatial organization of synaptic inputs along the dendritic tree of single V1 neurons. The results from this project will provide insights into the input – output relationship of a neuron to visual stimuli, namely how the visual response properties of synaptic inputs impinging onto a given neuron combine to give rise to the response of that neuron to visual stimuli.

Malcolm L. Gefter Jane Coffin Childs Fellow

MRC Center, University Medical School, England

Appointed in 1967

Walter J. Gehring Jane Coffin Childs Fellow

Yale University

Appointed in 1968

Margaret W. Geiger Jane Coffin Childs Fellow

Yale University

Appointed in 1976

Arne Gennerich Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2004

Norman E Genter Jane Coffin Childs Fellow

Stanford University

Appointed in 1968

Lisa N. Gentile Jane Coffin Childs Fellow

University of British Columbia, Vancouver

Appointed in 1996

Norman E. Gentner Jane Coffin Childs Fellow

Stanford University

Appointed in 1969

Naomi Genuth, Ph.D. Jane Coffin Childs - HHMI Fellow

University of California, Berkeley

Appointed in 2023

Aging is a complex physiological process coordinated across tissues within an organism. Loss of protein homeostasis is a hallmark of aging, yet it is not understood why dysregulation in protein synthesis occurs, and if this dysregulation drives aging pathologies. Dr. Naomi Genuth will investigate these questions in Dr. Andrew Dillin’s lab at the University of California, Berkeley. Dr. Genuth will use C. elegans to visualize protein synthesis patterns in vivo in different tissues during the aging process. Ultimately, Genuth aims to define the molecules that contribute to dysregulation of protein synthesis and see whether manipulation of these molecules can delay and/or prevent the aging process. Dr. Genuth’s research will improve our understanding of changes in protein synthesis during aging at the molecular, cellular, and organismal levels, and may reveal new therapeutic strategies for aging pathologies.

As a Ph.D. student in Dr. Maria Barna’s lab at Stanford University, Genuth investigated the role of translational regulation in gene expression. Specifically, she developed a quantitative roadmap of how ribosome composition changes during human embryonic stem cell differentiation. Dr. Genuth will now investigate protein synthesis during aging in Dr. Dillin‘s lab.

Susan A. Gerbi Jane Coffin Childs Fellow

Max-Planck Institute

Appointed in 1971

Perter J. Gergen Jane Coffin Childs Fellow

Princeton University

Appointed in 1982

John A. Gerlt Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1974

Rachel M. Gerstein Jane Coffin Childs Fellow

Stanford University

Appointed in 1991

George Ghanim, Ph.D. Jane Coffin Childs Fellow

MRC Laboratory of Molecular Biology

Appointed in 2021

Telomeres are repetitive nucleoprotein structures that protect the ends of linear eukaryotic chromosomes. Despite their importance, telomeres shorten at each round of cellular division due to an inherently incomplete replication process at DNA ends. This poses a threat to genome stability. The telomerase complex extends the telomeric repeats by processively copying from an internal template sequence, thereby counterbalancing telomere shortening. The action of telomerase at the telomeres is highly regulated in the cell. The current evidence indicates that a protein complex called shelterin orchestrates telomerase recruitment and activity at the telomeres. In mammals, shelterin is a six-subunit complex that binds telomeric DNA repeats and recruits telomerase through its TPP1 subunit, which assembles as a heterodimer with POT1. TPP1-POT1 not only recruit telomerase, but also stimulates its processivity. Stimulation and recruitment by shelterin are essential for telomerase function in vivo, yet the structural basis of telomerase-shelterin interactions and shelterin-mediated telomerase processivity remains elusive. We determined the cryo-EM structures of telomeric DNA-bound telomerase in complex with TPP1 and with TPP1-POT1 at 3.2 Å and 3.9 Å resolution, respectively. These structures define the molecular interactions between telomerase and TPP1-POT1 required for telomerase recruitment to telomeres. The interaction with TPP1-POT1 stabilizes the DNA, revealing an unexpected path exiting the active site and a conserved DNA anchor site on telomerase, which is important for telomerase processivity. Overall, our findings provide important insights into telomerase recruitment to telomeres and set a framework for future studies on telomerase regulation by shelterin.

Megha Ghildiyal Jane Coffin Childs Fellow

Carnegie Institute for Science

Appointed in 2011

Sourav Ghosh Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Appointed in 2002

Matthew C. Gibson Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2002

William Gibson Jane Coffin Childs - HHMI Fellow

California Institute of Technology

Appointed in 2012

Grace B. Gill Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1989

Peter J. Gillespie Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 2002

Thomas D. Gilmore Jane Coffin Childs Fellow

University of Wisconsin, Madison

Appointed in 1984

Christina Gladkova Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2019

Niall F. Glanville Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1978

Caleb Glassman, Ph.D. Jane Coffin Childs - HHMI Fellow

Brigham and Women's Hospital

Appointed in 2022

Viruses are obligate intracellular pathogens that shape host cell physiology to promote replication and spread. Viral infection is counterbalanced by the host immune response which attempts to detect and eliminate virally infected cells. To reproduce and evade immune detection, viruses modulate expression and post-translational modification of host proteins. The ubiquitin-proteasome system (UPS) mediates targeted degradation of proteins and consists of E1, E2, and E3 enzymes. The modular nature of the ubiquitin ligase pathway has led to co-option by pathogens which alter host protein stability in order to enhance replication and evade immune detection. Understanding how viruses manipulate the host cell proteome to promote infection and how these changes are detected by the immune system is central to the development of anti-viral therapies and vaccines. My postdoctoral research uses genetic and biochemical techniques to discover and dissect host-pathogen interactions with a focus on post translational modifications and their impact on cell signaling.

Alexander N Glazer Jane Coffin Childs Fellow

Weizmann Institute of Science, Israel /
University of Cambridge, England

Appointed in 1961

Kristin Gleitsman Jane Coffin Childs Fellow

Stanford University

Appointed in 2011

Robert H. Glew Jane Coffin Childs Fellow

Johns Hopkins University

Appointed in 1967

Bradley P. Glover Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2001

Yakov Gluzman Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 1977

Vasilena Gocheva Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2012

John B. Goetsch Jane Coffin Childs Fellow

Yale University

Appointed in 1947

Stephen P. Goff Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1978

Edward P. Gogol Jane Coffin Childs Fellow

Stanford University

Appointed in 1982

Marvin Gold Jane Coffin Childs Fellow

New York University

Appointed in 1962

David A. Goldberg Jane Coffin Childs Fellow

MRC Center, University Medical School, England

Appointed in 1984

Peter Goldmark Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1971

Michel Goldschmidt Jane Coffin Childs - Clermont Fellow

Stanford University

Appointed in 1981

Nitsan Goldstein, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2023

Medication for chronic pain often leads to addiction. Dr. Nitsan Goldstein thinks this may be because around one third of people experiencing chronic pain also suffer from anxiety. Additionally, anxiety is a strong predictor of chronic pain development. Dr. Goldstein predicts that targeting pain and pain-induced anxiety together may reduce chronic pain symptoms. She has identified neurons that are anxiolytic and will test their functional relationship with pain-induced anxiety and a chronic pain-like state. Goldstein will conduct her experiments in Dr. Fan Wang’s lab at the Massachusetts Institute of Technology. Dr. Goldstein hopes that investigating both the central and peripheral causes of chronic pain and anxiety will open avenues for more effective pain treatments.

As a graduate student in Dr. J. Nicholas Betley’s lab at the University of Pennsylvania, Goldstein investigated how the brain regulates food intake. Specifically, Dr. Goldstein discovered that the activation of hunger circuits enhances dopamine release, which is critical for motivating humans to seek rewards like food. These studies helped reveal new relationships between neural programs and have prepared Dr. Goldstein to investigate the relationship between chronic pain and anxiety.

Kent G. Golic Jane Coffin Childs Fellow

University of Chicago

Appointed in 1986

Jose Antonio Gomez Jane Coffin Childs Fellow

Stanford University School of Medicine

Appointed in 2014

Recent genome-wide sequencing studies have revealed that genes encoding subunits of SWI/SNF-like BAF complexes are among the most frequently mutated in human cancers. Indeed over 20% of all human cancers have mutations in the subunits of these complexes. I have found that oncogenic subunits of this complex also form a much larger 4 MDa assembly that has been unappreciated to date, raising the question of which assembly is mediating tumor suppression by these complexes. I have also found that this larger complex is characterized by the specific assembly of three subunits, which will allow me to specifically characterize this 4 MDa complex at a biochemical and genetic level. One of these subunits is BAF180 (PBRM1) and my initial results indicate oncogenic mutations in this complex dominantly interfere with the oligomerization of the complex, raising the intriguing model that BAF180 is the keystone subunit of this oncogenic complex. The hypothesis that the 4 MDa complex targets a unique repertoire of chromatin-mediated, tumor suppressor processes will be tested by mass spec and genome-wide analyses. The work I propose will lead to a mechanistic understanding of cancer susceptibility genetics in the context chromatin-mediated control of gene expression.

David K. Gonda Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1986

Venugopala R. Gonehal Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 1999

Juan E. Gonzalez Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1991

Peter N. Goodfellow Jane Coffin Childs Fellow

Stanford University

Appointed in 1976

Daniel Goodman Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2017

Immune dysregulation is implicated in a variety of diseases, and modulation of immune cell signaling has shown remarkable promise in the treatment of allergy, autoimmunity, and cancer. At the surface of each immune cell, hundreds of different receptors serve as the gateways through which information is recognized and integrated. These receptors are surprisingly modular and can be mutated and composed to rewire cellular inputs and outputs, as showcased by the success of cell-based genetic therapies like Chimeric Antigen Receptor T-cell (CAR-T) therapy._x000D_
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My work combines computational protein design, chemical DNA library synthesis, and high-throughput pooled screening of millions of genetically modified primary human immune cells, each with different synthetic receptors. We are measuring these cells for differences in proliferation, differentiation, activation, and localization, both in vitro and in animal models. A better understanding of the relationship between receptor sequence, signaling outcome, and cellular phenotype will lead to next-generation cell-based genetic therapies which manipulate the immune system to combat a variety of diseases.