Directory - Jane Coffin Childs Memorial Fund

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Year Appointed

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Michael M. Shen Jane Coffin Childs Fellow

Harvard University

Appointed in 1988

Zhongzhou Shen Jane Coffin Childs Fellow

Cleveland Clinic Foundation

Appointed in 1999

Jingshi Shen Jane Coffin Childs Fellow

Columbia University

Appointed in 2005

Koning Shen Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2017

Aging is a risk factor for nearly every chronic disease, and organismal health in aging and age-related disorders is increasingly linked to mitochondrial health. A key contributor to age-related mitochondrial dysfunction is the accumulation of misfolded proteins (or proteotoxic stress). Recent evidence has shown how proteotoxic stress can activate the unfolded protein response in mitochondria (UPRmt), a conserved stress response pathway critical for regulating longevity. However, the molecular mechanisms underlying UPRmt activation and lifespan extension during aging remain unknown. The objective of this proposal is to_x000D_
identify a framework for how mitochondria recognize and respond to proteotoxic stress, which will inform how stress response mechanisms become compromised during aging. First, we will investigate how age associated proteotoxic stress activates the UPRmt and how this mechanism becomes compromised during aging. Secondly, we will conduct a focused RNAi screen to discover novel downstream effectors of the UPRmt that are essential for protecting lifespan upon proteotoxic stress. By establishing the relationship between the UPRmt and proteotoxic stress in aging, we will gain a fundamental understanding of the molecular basis of mitochondrial aging. This will establish new realms of therapeutic intervention that directly target the underlying cause of nearly every chronic disease – getting older.

Thomas E. Shenk Jane Coffin Childs Fellow

Stanford University

Appointed in 1973

Kelly A. Shepard Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2001

Madeline Sherlock Jane Coffin Childs Fellow

University of Colorado, Anschutz Medical Campus

Appointed in 2019

My postdoctoral research is focused on structured viral RNAs involved in enhancing translation of viral proteins. Some of the RNAs I‚Äôm studying are able to induce a reinitiation event within the viral RNA genome through specific interactions with the ribosome. My research focuses on the determining the molecular interactions that enable this RNA structure to promote translation activity at downstream open reading frames following a translation termination event. Another set of RNAs I‚Äôm studying are found primarily in plant viruses and mimic cellular tRNAs. Previous and ongoing studies in the Kieft lab aim to determine how different examples of these tRNA-like structures fold, the structural and functional differences between different classes and subtypes, and how these RNAs enhance viral translation.

Lisa M. Shewchuk Jane Coffin Childs Fellow

University of Oregon

Appointed in 1990

Christine K. Shewmaker Jane Coffin Childs Fellow

National Institute for Medical Research, England

Appointed in 1979

Honglue Shi, Ph.D. Jane Coffin Childs - HHMI Fellow

University of California, Berkeley

Appointed in 2023

CRISPR-Cas enzymes are versatile tools for gene editing and research applications such as transcriptional regulation and imaging. The speed and accuracy of CRISPR-Cas enzymes are crucial, yet how they identify a unique ~ 20-base-pair target within billions of base pairs in the genome is still unclear. Dr. Honglue Shi aims to obtain a more quantitative and predictive understanding of how natural and engineered CRISPR-Cas enzymes rapidly and accurately target specific DNA sequences in Dr. Jennifer Doudna’s lab at the University of California, Berkeley. Shi will use structure-guided biochemistry to develop a kinetic model for CRISPR-Cas9 search speed and accuracy. He will then test the generality of the model on additional CRISPR enzymes and ancestral RNA-guided TnpB enzymes. This research is fundamental to understanding both the evolutionary history of RNA-guided enzymes and the utility of these systems for genome editing. In the future, these results will enable predictions and design of genome editing functions that are not possible or practical today and will greatly accelerate the field as well as the precision and outcomes of next-generation genome editing tools.

As a Ph.D. student in Dr. Hashim Al-Hashimi’s lab at Duke University, Shi focused on the development of biophysical approaches such as NMR spectroscopy to extend the description of nucleic acids from static structures to dynamic ensembles, which results in a deeper and more predictive understanding of how nucleic acids are being recognized by other biomolecules. Having developed this expertise in nucleic acid biophysics and perspectives in dynamic ensembles, Dr. Shi is ready to elucidate the properties that define the best genome editors in Dr. Doudna’s lab.

Ellen K. Shibuya Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1989

Myung K. Shin Jane Coffin Childs Fellow

Princeton University

Appointed in 1995

Jeoung-Sook Shin Jane Coffin Childs Fellow

Yale University

Appointed in 2004

David M. Shore Jane Coffin Childs Fellow

MRC Center, University Medical School, England

Appointed in 1982

Bing Shui Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2024

Tissue regeneration, in a normal developmental context, and cancer are both forms of cellular proliferation. However, tissue regeneration is regulated and responsive to the surrounding environment, whereas cancer sheds these restraints. Understanding the commonalities and the differences between tissue regeneration and cancer may provide insight into novel avenues for cancer therapeutics.

Dr. Bing Shui will investigate the role of tissue damage in facilitating the early pre-neoplastic to neoplastic transition in colorectal cancer in Dr. Tyler Jacks’ lab at the Massachusetts Institute of Technology. Dr. Shui will examine how tissue damage cooperates with oncogenic mutations to initiate cancer. He will also compare damaged mutant and wildtype cells to identify vulnerabilities that can be leveraged to selectively destroy precancerous cells. Ultimately, a better understanding of the role of tissue damage in this early precancerous transition may reveal novel prophylactic cancer treatments.

Shui’s interest in the relationship between tissue regeneration and cancer burgeoned in Dr. Kevin Haigis’ lab at Harvard University. During his Ph.D. studies, he examined the role of microRNAs (miRNAs) in colon regeneration and colon cancer. First, Shui demonstrated that miRNAs are required for tissue regeneration and miRNA suppression exacerbated colon damage due to failed regeneration. Next, he examined the role of miRNAs in colon cancer and discovered a novel form of posttranslational regulation mediated by oncogenic K-Ras that governs global miRNA function. Now Shui will use his expertise in tissue damage and regeneration to identify vulnerabilities in colorectal cancer during his postdoctoral research.

Howard A. Shuman Jane Coffin Childs Fellow

Harvard University

Appointed in 1979

Richard Shutt Jane Coffin Childs Fellow

Stanford University

Appointed in 1972

Kausik Si Jane Coffin Childs Fellow

Columbia University

Appointed in 2000

Matthew Sieber Jane Coffin Childs Fellow

Carnegie Institute for Science

Appointed in 2012

Ruth B. Siegel Jane Coffin Childs Fellow

University of Wisconsin

Appointed in 1972

Vivian Siegel Jane Coffin Childs Fellow

Max-Planck Institute /
University of California

Appointed in 1988

Miriam L. Siekevitz Jane Coffin Childs Fellow

University of Cologne, Germany

Appointed in 1982

Ethan R. Signer Jane Coffin Childs Fellow

Institut Pasteur, France

Appointed in 1965

Thomas J. Silhavy Jane Coffin Childs Fellow

Harvard University

Appointed in 1975

Marion Silies Jane Coffin Childs Fellow

Stanford University

Appointed in 2010

My current research interest is visual system function in fruit flies. I want to understand how different behaviorally relevant visual cues, such as motion or polarized light information, are processed in the Drosophila brain.

I am from Germany. I studied biology and chemistry at the University of M√ºnster, where I worked in a plant pathology lab as an undergraduate; I also did internships at Washington State University and Edinburgh University. ¬†During that time I became interested in neuroscience and subsequently studied the development of the nervous system for my diploma thesis and PhD at the Department of Neurobiology in M√ºnster. I used the fly embryonic peripheral nervous system to study how neurons and glial cells communicate in order to coordinate axonal outgrowth with glial cell migration. For my postdoc I switched from developmental to functional aspects of neuroscience. Outside the lab, I enjoy exploring the Bay area on my road bike or hiking, and meeting friends.

Antonio Sillero Jane Coffin Childs Fellow

New York University

Appointed in 1970

Justin Silpe, Ph.D. Jane Coffin Childs - HHMI Fellow

Princeton University

Appointed in 2021

DNA-damaging agents are the pervasive inducers of temperate phages in model bacteria. Most bacteria in the biosphere are polylysogens, harboring multiple prophages. Thus, how co-residing prophages compete for cell resources if they all respond to an identical trigger is unknown. My project in the Bassler Lab is focused on the discovery of regulatory modules that control prophage induction independently of the DNA damage cue. The modules I uncovered lack sequence similarity but share regulatory logic by having a transcription factor that activates the expression of a neighboring gene encoding a small protein. The small protein inactivates the master repressor of lysis, leading to induction. Polylysogens harboring two prophages exposed to DNA damage release mixed populations of phages. Single-cell analyses reveal that this blend is a consequence of discrete subsets of cells producing one, the other, or both phages. By contrast, induction via the DNA-damage-independent module results in cells producing only the phage sensitive to that specific cue. Thus, in the polylysogens tested, the cue used to induce lysis determines phage productivity. Considering the lack of potent DNA-damaging agents in natural habitats, additional phage-encoded sensory pathways to lysis could play fundamental roles in phage-host biology and inter-prophage competition.

Allen E. Silverstone Jane Coffin Childs Fellow

University of Edinburgh, Scotland

Appointed in 1970

Daniel T. Simmons Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1974

Jeffrey A. Simon Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1987

Miljan Simonovic Jane Coffin Childs Fellow

Yale University

Appointed in 2003

Harinder Singh Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1984

Ila Singh Jane Coffin Childs Fellow

University of California, San Francisco /
Stanford University

Appointed in 1993

Niladri K. Sinha Jane Coffin Childs - HHMI Fellow

Johns Hopkins University School of Medicine

Appointed in 2018

Translational elongation is a tightly regulated process, whose dysfunction triggers cellular quality control (QC) processes that minimize production of defective protein molecules. Aberrantly stalled ribosomes on messenger RNAs (mRNAs) disrupt translational homeostasis and arise as a consequence of inefficient decoding, defective mRNAs, and cellular insults, such as stress and starvation. As such, the primary role of co-translational QC is to initiate ribosomal rescue by splitting the ribosomal subunits, triggering mRNA decay, and enabling recycling of the subunits for new rounds of translation. _x000D_
The molecular cues required to initiate ribosomal QC (RQC) are poorly characterized, as are the fate of ribosomes affected by RQC. Using a combination of biochemical, mass-spectrometric and ribosome profiling approaches, I am studying how QC factors spatiotemporally recognize and resolve stalled ribosomes and how such factors discriminate terminally (or “dead end”) stalled ribosomes on defective mRNAs, from transiently paused ribosomes on elongation-limited transcripts. _x000D_

Ayesha Sitlani Jane Coffin Childs Fellow

Yale University

Appointed in 1993

Rufus E. Skillern Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1973

Gary M. Skinner Jane Coffin Childs Fellow

University of Arizona

Appointed in 2002

Arthur I. Skoultchi Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1970

Thomas J. Smith Jane Coffin Childs Fellow

Purdue University

Appointed in 1986

Francine R. Smith Jane Coffin Childs Fellow

University of North Carolina

Appointed in 1987

Elenoe Smith Jane Coffin Childs Fellow

Boston Children's Hospital

Appointed in 2013

This project aims to identify cellular mechanisms contributing to elevation of fetal hemoglobin (HbF, ?2?2) levels, the most promising therapy for patients with sickle cell disease. The characterization of BCL11A, a repressor of HbF production, and potential BCL11A targets within the ?-globin locus, will impact therapy design and treatment of the major hemoglobin disorders whose global health burden is rising. Although BCL11A is dispensable for normal red cell function, studies in mice have determined that it is required for development, presenting a potential obstacle for therapies designed to inhibit BCL11A function by small molecule. Aim1 will determine the dependence of BCL11A erythroid expression on a single nucleotide polymorphism dense region, identified by genome wide association studies. Aim2 will identify a region required for ?-globin gene repression within the A?-? intergenic region of the ?-globin locus. Both aims will utilize DNA targeting of mouse embryonic stem cells and analysis of BCL11A expression and/or globin gene expression in fetal and adult mice. These studies will contribute to a fuller understanding of ?-globin gene regulation, provide in vivo models for molecular characterization of hemoglobin switching, and identify erythroid specific targets for therapeutic intervention.

H. Ralph Snodgrass Jane Coffin Childs Fellow

Institute for Cancer Research

Appointed in 1981

Christopher D. Snow Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2006

Loren R. Snyder Jane Coffin Childs Fellow

International Laboratory of Genetics and Biophysics, Italy /
Institut de Biologie Physico-Chimique, France

Appointed in 1968

Adam Wei Jian Soh, Ph.D. Jane Coffin Childs Fellow

Duke University

Appointed in 2023

Dr. Adam Wei Jian Soh will investigate how the basement membrane (BM), a sheet-like extracellular matrix that encloses tissues, stretches in mechanically-active tissues in Dr. David Sherwood’s lab at Duke University. Dr. Soh will use C elegans ovulation as a novel model system for examining BM stretching and recovery. Soh has performed a localization screen and identified candidate proteins that are likely important for BM dynamics. He will follow up on these findings by determining which proteins are functionally important for the stretching and recovery of BMs. Soh hypothesizes that type IV collagen is critical for stretching tissues as genetic defects in this gene lead to vasculature hemorrhaging and muscle dysfunction. This research may also identify novel genes that are critical for tissue support and are mutated in human disease.

Previously, Dr. Soh investigated the mechanics of motile cilia beating as a PhD student in Dr. Chad Pearson‘s lab at the University of Colorado Anschutz Medical Campus. Specifically, he discovered a novel intracellular mechanism involving the cortical cytoskeleton network that regulates cilia beating synchronization. Through this research Soh developed expertise in imaging techniques and cellular biophysics. This experience has prepared Dr. Soh for his current project dissecting basement membrane dynamics.