Directory - Jane Coffin Childs Memorial Fund

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Stephen P. Goff, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Isolation and characterization of MuLV mutants

Edward P. Gogol, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Electron microscopy of gap junctions

Marvin Gold, Ph.D. Jane Coffin Childs Fellow

Albert Einstein College of Medicine

Project Title: Nucleic acid synthesis

David A. Goldberg, Ph.D. Jane Coffin Childs Fellow

Medical Research Council (MRC),UKRI

Project Title: Genetic analysis of Drosophila eye development

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

Harvard Medical School

Project Title: Nerve tissue culture

Image of Michel Goldschmidt-Clermont, Ph.D.

Michel Goldschmidt-Clermont, Ph.D. Clermont-Jane Coffin Childs Fellow

Stanford University

Project Title: Chromosome structure and gene expression

Nitsan Goldstein, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Central control of the autonomic nervous system in chronic pain and anxiety

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, Ph.D. Jane Coffin Childs Fellow

University of Chicago

Project Title: Role of hsp70 in the heat shock response of Drosophila

Jose Antonio. Gomez, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Characterization of a novel 4 Mda oncogenic complex

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, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Function and regulation of yeast ubiquitin

Venugopala R. Gonehal, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Cell-cell interactions and regulation of cell division in floral meristems of A thaliana

Juan E. Gonzalez, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Role of oligosaccharides in Rhizobium symbiosis

Peter N. Goodfellow, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Antigens found on mouse embryos and teratocarcinomas

Daniel B. Goodman, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Mapping and manipulating T-cell plasticity via synthetic receptor libraries

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.

Aubrey Gorbman, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Metabolism of radioactive iodine in lower chordates and the problem of homology of the thyroid gland

Julius Gordon, M.D. Jane Coffin Childs Fellow

Chester Beatty Research Institute, England

Project Title: Attempt to prepare potent antisera against antigens of the grafts

Jack Gorski, Ph.D. Jane Coffin Childs Fellow

University of Glasgow

Project Title: Isolation of the myeloma heavy chain genre

Max E. Gottesman, M.D., Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Attempt to identify and isolate the enzyme responsible for the synthesis of complementary strands of DNA

Susan Gottesman, Ph.D. Jane Coffin Childs Fellow

National Cancer Institute

Project Title: Enzyme systems of bacteriophage lambda in vitro

Hannah J. Gould, Ph.D. Jane Coffin Childs Fellow

University College, London

Project Title: Hemoglobin synthesis

Kathleen L. Gould, Ph.D. Jane Coffin Childs Fellow

University of Oxford

Project Title: Analysis of protein kinases regulating cell growth

Richard L. Gourse, Ph.D. Jane Coffin Childs Fellow

Brown University

Project Title: Control of ribosome synthesis after alteration of genes for rRNA

Lakshmi Goyal, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Functional and mutational analysis of Drosophila IAP's

Yogesh Goyal, Ph.D. Jane Coffin Childs Fellow

University of Pennsylvania

Project Title: Cellular states guiding plasticity and reprogramming paradigms in cancer

Resistance to therapy is a hallmark of many cancers (e.g. melanoma). Advancements in quantitative single-cell biology has allowed characterization of pre- and post-therapy melanoma cells with unprecedented resolution. Specifically, recent studies have demonstrated that rare populations of preresistant melanoma cells exhibit non-genetic plasticity such that they occupy a transient state capable of withstanding drug treatment, but can be reprogrammed into a stable drug-resistant state upon drug addition. While this provides novel opportunities to tackle resistance, we still lack information on different cellular states and the underlying molecular mechanisms of transition between states. The first aim of this proposal is to develop a theoretical and conceptual understanding on the origins of transient, rare preresistant populations. The second aim focusses on developing an experimental data-driven computational framework to dissect the genetic networks in the pre- and post-resistant states. The last aim proposes developing stochastic population dynamics models to track cells at multiple timescales, and inform on rational drug dosing strategies. The eventual goal is to integrate the network models with the population level model, thus allowing multiscale analysis of regulation in melanoma. Together, my work will develop quantitative frameworks to systematically characterize the cellular landscapes guiding plasticity and reprogramming paradigms for therapy resistance.

Thomas H. Graf, Ph.D. Jane Coffin Childs Fellow

Duke University

Project Title: Characterization of mutants of Rous sarcoma virus

Thomas GW. Graham, Ph.D. Merck-Jane Coffin Childs Fellow

University of California, Berkeley

Project Title: In Vivo single-molecule imaging of enhancer-promoter communication

The different cell types in our body have an incredible variety of sizes, shapes, and functions, despite having the same genome. Differences between cell types arise from differences in which genes are transcribed into RNA. Transcription is regulated by DNA sequences called enhancers, which in some cases are located hundreds of thousands of basepairs away from their target genes. While we know the identities of many of these enhancers, and the proteins that bind to them, we lack a coherent model of how enhancers regulate transcription. Various lines of evidence suggest that large protein complexes form a bridge between enhancers and their target promoters. However, we lack a basic understanding of the composition, size, and internal organization of these enhancer-promoter complexes. Important questions are: 1) How many copies of different proteins assemble at enhancers and promoters? 2) What protein-protein and protein-DNA interactions are important for assembling enhancer-promoter complexes? 3) How dynamic are these complexes? 4) How do enhancer-promoter complexes ultimately regulate transcription? To address these questions, I am working to develop new fluorescence imaging approaches in live cells, which will combine fluorescent labeling of DNA, RNA, and protein with new technologies such as single-molecule tracking and lattice light sheet microscopy.

Robert M. Grainger, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Molecular mechanisms of chromosome elimination in Ascaris lumbricoides

Jay D. Gralla, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Transcriptional control of catabolite-sensitive gene expression

Adam Granger, Ph.D. HHMI-Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Multilingual neurons: GABA corelease from cholinergic basal forebrain neurons

Neurons are typically thought to release a single fast neurotransmitter, though a growing number of examples of neurotransmitter corelease are being discovered. Our lab has found preliminary evidence that the acetycholine (ACh) releasing neurons of the basal forebrain (BF) also release GABA. The BF is the primary source of Ach neurotransmission throughout the central nervous system, and is responsible for modulating attention, arousal, and the cognitive deficits that underlie Alzheimer’s disease. In this proposal, I outline a research plan to characterize the extent of GABA/ACh corelease from BF neurons throughout the cortex. I will then explore the presynaptic mode of ACh/GABA corelease to determine if they are released from the same or separate populations of synaptic vesicles. Finally, I will test the functional importance of this projection in shaping cortical activity by performing in vivo recordings from the cortex awake, behaving mouse during optogenetic activation of ACh-releasing BF neurons. The contribution of GABA will be explored by comparing recordings from wild-type mice with mice that lack GABA release specifically in ACh-releasing BF neurons. The results of these experiments will provide novel insight into the role of GABA/ACh corelease for BF function.

Brenton R. Graveley, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: The role of SR proteins in splicing enhancer function

William D. Graziadei, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Peptide chain synthesis

Ethan Greenblatt, Ph.D. Jane Coffin Childs Fellow

Carnegie Institution for Science

Project Title: Understanding nuclear aging in the Drosophila follicle stem lineage

Aging is characterized by a progressive decline in tissue physiology. The reasons for this decline, whether antagonistic pleiotropy, error catastrophe, or developmental programming, have been difficult to pinpoint. Likewise, which cell types and subcellular components are the most important targets of decline remain hotly debated. I have long been interested in aging despite its acknowledged difficulty as a research topic. The submitted proposal describes my strategy for testing ideas and approaches that I believe have the potential to greatly advance this field, and to launch my career as an independent investigator. My approach involves a novel system in which to study aging – the Drosophila follicle stem cell lineage, and a novel hypothesis regarding a primary target of the aging process – the epigenetic system of the cell nucleus.

Arno L. Greenleaf, Ph.D. Jane Coffin Childs Fellow

University of Heidelberg

Project Title: Eukaryotic transcription using antibodies prepared against eukaryotic RNA polymerases

Iva S. Greenwald, Ph.D. Jane Coffin Childs Fellow

Medical Research Council (MRC),UKRI

Project Title: Molecular analysis of the unc-93 locus of C. elegans

Helen A. Greer, Ph.D. Jane Coffin Childs Fellow

Cornell University

Project Title: Genetic regulation in S. cerevisiae

Charles Gregoire, M.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Nutritional requirements of lymphoid tissues, including lymphoid tumors

Carlo Gregolin, M.D. Jane Coffin Childs Fellow

New York University

Project Title: Research on liver enzyme, acetyl CoA

Lydia M. Gregoret, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Elucidating the determinants of protein folding

Richard I. Gregory, Ph.D. Jane Coffin Childs Fellow

The Wistar Institute /
The Wistar Institute

Project Title: Heterochromatin remodeling by ISNI-containing complexes

Linda C. Griffin, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Identification of tRNA synthetase editing active site

Abigail F. Groff, Ph.D. Jane Coffin Childs Fellow

Whitehead Institute

Project Title: Sexually dimorphic gene expression in human preimplantation development

Abbie Groff studies sex differences at the earliest stages of development in Dr David Page’s laboratory at the Whitehead Institute.

Differences between the sexes start only a few cell divisions after conception. XY (‘male’) embryos tend to develop more quickly than XX (‘female’) embryos, reaching the blastocyst stage faster and with more cells. Prior studies have also reported various metabolic differences between the sexes in preimplantation development across multiple mammalian species. Since these cells have never been exposed to sex hormones, and the conditions of their culture are highly controlled, these differences must be due to the gene content and regulatory influence of the sex chromosomes. However, the transcriptional underpinnings of these differences are unclear.

Abbie’s work focuses on characterizing gene expression differences between 46,XX and 46,XY cells in preimplantation human development at single-cell resolution. Using this system, Abbie seeks to understand the specific contributions of the sex chromosomes to gene expression during the first cell divisions, and also chart the influence of nascent X chromosome inactivation on genome-wide expression changes.

Beyond explaining current “known” physiological sex differences at this developmental stage, she anticipates this work may provide insight into the development of sex biased phenotypes at later developmental stages, such as the predominance of disorders of placental dysfunction, including pre-eclampsia, in pregnancies with a male fetus.

Eduardo A. Groisman, Ph.D. Jane Coffin Childs Fellow

Scripps Research Institute

Project Title: Molecular genetics of intracellular parasitism

Yoram Groner, Ph.D. Jane Coffin Childs Fellow

Albert Einstein College of Medicine

Project Title: RNA synthesis in RNA tumor viruses

Lawrence I. Grossman, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Mitochondrial DNA

Alexandra T. Grote, Ph.D. Jane Coffin Childs Fellow

Broad Institute

Project Title: Pioneering comparative regulomics to probe mechanisms of chronic salmonella

Joshua Gruber, M.D., Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Integrated omics of malignant transformation by breast cancer genes

Through my clinical work with oncology patients I became acutely aware of how few interventions we are able to offer patients to prevent cancer. Even patients with inherited syndromes that confer a near-certainty of developing cancer have few, often unappealing, options to actually prevent cancer. This motivated me to investigate molecular mechanisms of the earliest steps of malignant transformation. I chose to study the genes causing inherited breast cancer because each one constrains the malignant phenotype of breast cells, an effect that can be modeled in vitro._x000D_
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These ideas led me to team up with my advisor Dr. Michael Snyder at Stanford who has pioneered multiple high-throughput omics technologies to densely profile biological systems. These tools allow for an unprecedented window into cellular dynamics driving malignant transformation. I am particularly interested in how genomic aberrations in non-coding DNA elements can unlock transcriptional programs that drive malignancy. The hope is to uncover molecular switches that can be targeted to prevent cancer onset.

Liangcai Gu, Ph.D. HHMI-Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Developing cell-free platform for biosynthesis and metabolic engineering of cancer therapeutics

Current research: Developing a next-generation protein display technology which allows high-throughput screening of gene functions and protein-protein interactions by coupling the cell-free protein synthesis, high-resolution imaging and next-generation DNA sequencing technologies.

I received my B.S. in chemistry and my M.S. in biochemistry and molecular biology in my home country of China, and my Ph.D. in medicinal chemistry in 2008 from the University of Michigan. Between 2004 and 2009, working with Professor David Sherman, I identified and characterized a whole set of novel enzymes involved in the curacin A biosynthesis. Currently, I am learning DNA tricks in Professor George Church¬ís lab. I am deeply interested in both technology development and answering fundamental biological questions, and look forward to a synergy between them in my future career.

Leonard P. Guarente, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: Expression of sea urchin histone genes in E. coli

Chantal K. Guegler, Ph.D. Merck-Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Uncovering the regulation and function of nuclear mRNA degradation

mRNA degradation is an important step in gene expression that is traditionally thought to occur in the cytoplasm. However, a recent genome-wide study uncovered a class of genes whose transcripts are predicted to be primarily degraded in the nucleus. Yet, it is unclear how and why these mRNAs undergo nuclear degradation. Dr. Chantal Guegler will use both candidate- and screening-based approaches to determine which pathways are important for nuclear mRNA degradation, and how this process influences cellular physiology. Dr. Guegler will conduct this research in Dr. Stirling Churchman’s lab at Harvard Medical School. This work will reveal the key determinants of nuclear mRNA degradation and how this process contributes to gene expression regulation.

As a graduate student, Guegler studied bacterial toxin-antitoxin (TA) systems and their role in protecting against bacteriophage infection in Dr. Michael Laub’s lab at the Massachusetts Institute of Technology. There, Dr. Guegler demonstrated that the RNase toxin ToxN cleaves phage mRNAs to disrupt the translation and assembly of viral particles. Interestingly, Guegler also demonstrated that T4 phage can combat ToxN using the phage-encoded antitoxin TifA that sequesters RNA-bound ToxN to prevent it from degrading additional phage mRNAs. With her background in RNA degradation in bacterial TA systems, Dr. Guegler will now investigate nuclear mRNA degradation in eukaryotic cells.

Gregory M. Guild, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Eukaryotic gene transcription

Shawna Guillemette, Ph.D. Jane Coffin Childs Fellow

Brigham and Women's Hospital

Project Title: The role of SASP regulator GATA4 in senescence and cancer

The majority of cancer therapeutics currently used result in DNA damage that can trigger cell death or senescence in cancer cells and in healthy neighboring cells. Understanding how transformed cells and otherwise healthy cells induce or evade senescence pathways in response to cancer therapies is the major interest of my research in order to better understand therapeutic resistance mechanisms._x000D_
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I was born and raised in New Hampshire and received my BS in biochemistry from the University of Vermont. My research career started in Jim Vigoreauxs lab where I investigated mechanisms of energy transport in Drosophila flight muscle. As a graduate student in Sharon Cantors lab at the University of Massachusetts Medical School I studied DNA repair pathways and mechanisms that lead to chemo-resistance in hereditary forms of ovarian cancer. Currently, I am working with Dr. Stephen Elledge in the Department of Genetics at Harvard Medical School. Here I aim to elucidate the molecular circuitry that controls cellular senescence.