Directory - Jane Coffin Childs Memorial Fund

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Margaret T. Fuller, Ph.D. Jane Coffin Childs Fellow

Indiana University

Project Title: Genetic and biochemical analysis of tubulin function in Drosophila

Bernard K. Fung, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Energy transfer

Andrew J. Furley, Ph.D. Jane Coffin Childs Fellow

Columbia University

Project Title: Molecular characterization of TAG-1

Nadezda Fursova, Ph.D. Jane Coffin Childs Fellow

National Cancer Institute

Project Title: Enhancer transcription dynamics and its role in gene activation

Enhancers are distal cis-regulatory elements that control precise execution of transcriptional programs during development and in response to external stimuli. How enhancers find and activate their target genes, and what molecular activities are required for enhancer function remains a central outstanding question in the field. Recent advances in nascent RNA-sequencing uncovered widespread transcription from enhancers, which has become widely recognized as a robust signature of enhancer activity. However, mechanistic understanding of enhancer transcription, its regulation and, most importantly, functional role in gene activation is currently missing.
In my work, I aim to address these fundamental questions by using single-molecule and live-cell imaging approaches to characterize the intrinsic dynamics of enhancer transcription in single cells. To generalize my conclusions from individual enhancers to a genome scale, my ultimate goal is to develop high-throughput single-molecule approaches for systematic characterization of enhancer transcription. Using these new tools, I will investigate how transcription at enhancers and their target gene promoters is coordinated at the single-cell level to discover if these processes are functionally linked. Together, this work will be an essential step towards a deeper mechanistic understanding of enhancer function in gene activation and how enhancer perturbations can lead to severe developmental disorders and cancer.

Mark E. Furth, Ph.D. Jane Coffin Childs Fellow

Medical Research Council (MRC),UKRI

Project Title: Differentiation of hemopoietic cells

Deborah K. Fygenson, Ph.D. Jane Coffin Childs Fellow

University of Southern California, Los Angeles

Project Title: The biochemical basis of DNA synthesis fidelity

Eric A. Galburt, Ph.D. Agouron-Jane Coffin Childs Fellow

Lawrence Berkeley National Laboratory /
University of California, Berkeley

Project Title: Mechanochemistry of transcription-couple DNA repair

Maria E. Gallegos, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Activity-dependent axon outgrowth: a genetic approach

Alison E. Gammie, Ph.D. Jane Coffin Childs Fellow

Princeton University

Project Title: DNM1, a dynamic-related gene, participates in endosomal trafficking in yeast

Alexandra Gampel, Ph.D. Jane Coffin Childs Fellow

University of Cambridge

Project Title: Comparative studies of developmental mechanisms

Ninghai Gan, Ph.D. HHMI-Jane Coffin Childs Fellow

University of Texas Southwestern

Project Title: Role of two pore channels in NAADP-induced Ca2+ signaling

Barry S. Ganetzky, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Genetic studies of behavior in Drosophila

Margaret L. Gardel, Ph.D. Jane Coffin Childs Fellow

Scripps Research Institute

Project Title: Mechanical feedback in cell motility

Zev J. Gartner, Ph.D. Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: The role of tuberculosis sulfatases in virulence

Shimon Gatt, Ph.D. Jane Coffin Childs Fellow

Public Health Research Institute of the City of New York

Project Title: Pathways of Carbohydrate metabolism

Elizabeth R. Gavis, Ph.D. Jane Coffin Childs Fellow

Whitehead Institute

Project Title: Drosophila development

Laura Gaydos, Ph.D. Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Project Title: Uncovering mechanisms that control cell sorting during development

With a high prevalence of sugar in our society, especially in the form of sugar-sweetened drinks, it is important to understand the relationships between sugar metabolism and critical events in cancer progression. Recent research shows that sugar metabolism can promote oncogenesis in cell culture models of breast epithelial cells. This research was done with the sugar glucose, but breast cancer cells also have the unique ability to uptake fructose, while normal breast epithelial cells do not. Fructose and glucose are both simple sugars that are present in equimolar amounts in most of the food we eat. Although fructose is naturally found in fruits and vegetables, it is also added as high fructose corn syrup to many drinks and processed foods. More research needs to be done on how cancer cells respond to conditions with fructose and glucose. I am using breast cancer cell culture models to investigate the effects fructose and glucose have on cancer cell growth. By focusing on differences in regulation of gene expression with exposure to different sugars, we aim to discover the mechanisms fructose uses to fuel cancer cell growth. We hope this work will lead to better informed dietary recommendations for breast cancer patients and those with an increased risk for breast cancer.

Liang Ge, Ph.D. HHMI-Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: The origin of the autophagosomal membrane

XinXin Ge, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Cortico-

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.

Hui Ge, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Cofactors for mammalian transcriptional activators

Malcolm L. Gefter, Ph.D. Jane Coffin Childs Fellow

Medical Research Council (MRC),UKRI

Project Title: Molecular genetics and biochemistry of RNA

Walter J. Gehring, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Genetic mechanisms which control embryonic development

Margaret W. Geiger, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Transient vs stable membrane protein complexes

Arne Gennerich, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: The processive mechanism of kinesin motors

Lisa N. Gentile, Ph.D. Jane Coffin Childs Fellow

University of British Columbia

Project Title: Intramolecular inhibition of DNA binding of the Ets-1 ETS domain

Norman E. E.. Gentner, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: tRNA recognition

Norman E. Gentner, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: tRNA recognition

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

University of California, Berkeley

Project Title: The role of ribosome stalling in the regulation of longevity

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

Project Title:

Peter John J. Gergen, Ph.D. Jane Coffin Childs Fellow

Princeton University

Project Title: Marking genetic mosaics directly in late embryos

John A. Gerlt, Ph.D. Jane Coffin Childs Fellow

National Institutes of Health

Project Title: Kinetic study of staphylococcal nuclease fragments

Rachel M. Gerstein, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Lymphoid v(D)J recombination

George Ghanim, Ph.D. Jane Coffin Childs Fellow

Medical Research Council United Kingdom

Project Title: Structural studies of human telomerase and telomere-telomerase complexes

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, Ph.D., MBA Jane Coffin Childs Fellow

Carnegie Institution for Science

Project Title: Repair and regeneration of Drosophila musculature: a potential role for muscle stem cells

Sourav Ghosh, Ph.D. Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Project Title: Role of aPKC in cell migration during neurulation

Matthew C. Gibson, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Molecular-genetic analysis of squamous epithelial morphogenesis

William T. Gibson, Ph.D. HHMI-Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Investigation of a shadow response

Grace B. Gill, Ph.D. Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: Mechanism of transcriptional activation by Sp1

Peter J. Gillespie, Ph.D. Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Project Title: Establishment of sister chromatid cohesion

Thomas D. Gilmore, Ph.D. Jane Coffin Childs Fellow

University of Wisconsin, Madison

Project Title: Transformation by Rev-T

Christopher Giuliano, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Tracking and perturbing metabolic exchanges in cancer

What does microbial metabolism have to do with finding cancer therapies? Dr. Chris Giuliano thinks studying how microbes share and trade nutrients can help reveal novel ways to treat cancer. His goal is to find important metabolic “give-and-take” interactions between tumors and healthy tissues that could be targeted with drugs.

As a graduate student in Sebastian Lourido, Ph.D.’s lab at the Whitehead Institute for Biomedical Research, Giuliano studied the parasite Toxoplasma gondii. Because very little of its genome had been tested for genes that help it cause disease, he used a genome-wide CRISPR screen during infection and identified 300+ previously unknown virulence factors. He then studied three of these genes in depth and suggested a possible way to block infection.

Now as a Jane Coffin Childs Fellow in Kivanç Birsoy’s lab at The Rockefeller University, Giuliano will shift his focus to metabolic exchange across human organs. He wants to create an unbiased method to detect metabolic exchange between organs and tissues, using an idea inspired by microbial metabolism. He will apply this novel approach to cancer—studying how tumors interact metabolically with nearby cells, with immune cells, and even with distant organs—to uncover metabolic vulnerabilities that could be disrupted for therapy.

Christina Gladkova, Ph.D. HHMI-Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Understanding mitochondrial trafficking: linking mitochondria to motors

Niall F. Glanville, Ph.D. Jane Coffin Childs Fellow

University of Washington

Project Title: Regulation of expression of ovalbumin gene

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

Harvard Medical School/Brigham and Women's Hospital

Project Title: Viral manipulation of ubiquitin signaling

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.