Directory - Jane Coffin Childs Memorial Fund

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Year Appointed

Institution

Name

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Kerry S. Bloom Jane Coffin Childs Fellow

University of California, Santa Barbara

Appointed in 1980

David E. Boettiger Jane Coffin Childs Fellow

Imperial Cancer Research Fund Laboratories, England

Appointed in 1972

Aparna B. Bohil Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2007

Kenneth A. A. Bohnert Jane Coffin Childs Fellow - Calico

University of California, San Francisco

Appointed in 2014

The survival of a species requires that age must be reset with each generation. How germ cells, the reproductive cells of animals, accomplish this feat remains a fundamental, unsolved question in biology.

Utilizing the genetically-tractable nematode¬†Caenorhabditis elegans,¬†my research aims to identify mechanisms that cleanse the germ lineage of cellular damage and thereby allow for trans-generational rejuvenation. As a JCC fellow in Dr. Cynthia Kenyon’s lab, I have uncovered a regulatory switch that links damage elimination to fertilization and establishes a clean slate for the next generation prior to embryogenesis. Currently, I am exploring the molecular underpinnings of this switch in more detail.

Because molecules that ensure the immortality of the germ lineage might be capable of rejuvenating diverse cell types, I am also testing whether these natural age-reversal strategies can be co-opted in somatic tissues. If so, mechanisms important for germline immortality might provide a promising entry point for reversing whole-organism aging.

Alexandro Bolze Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2014

David Booth Jane Coffin Childs - Simons Foundation Fellow

University of California, Berkeley

Appointed in 2015

The evolution of regulatory mechanisms to coordinate multicellular development was critical to the origin of animals. Fundamental mechanisms that led to animal multicellularity may also be conserved in the closest living relative of animals, the choanoflagellates, since one species, Salpingoeca rosetta, can transition to a multicellular form called a rosette in a process that is reminiscent of early embryogenesis in animals. To uncover how this multicellular transition is controlled in S. rosetta, we are establishing transgenic and genomic methods that will enable investigating how genes coordinate rosette development. These advances will provide essential tools for exploring the molecular biology of these ecologically and evolutionarily important organisms and potentially illuminate the earliest stages of animal evolution and development.

William R. Boram Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1974

Marcus W. Bosenberg Jane Coffin Childs Fellow

University of Wisconsin, Madison

Appointed in 1994

Alfred L.M. Bothwell Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1975

Margot Bowen Jane Coffin Childs Fellow

Stanford University School of Medicine

Appointed in 2014

The p53 protein is a transcription factor that becomes activated in response to various cellular stress cues. Once activated, p53 induces target genes involved in apoptosis, cell cycle arrest, senescence and differentiation. Maintaining the correct levels of p53 is critical, since loss of p53 promotes cancer, while increased p53 activity promotes developmental defects and premature aging. To further define the consequences of increased p53 activity, the Attardi lab created a novel mouse model in which p53 is activated during embryogenesis. Intriguingly, this led to a variety of craniofacial and cardiovascular defects. This unique constellation of phenotypes is reminiscent of human CHARGE syndrome, which is caused by mutations in CHD7. I am now using our p53 mouse models to study the cellular and molecular mechanisms by which p53 promotes features of CHARGE syndrome. These studies will further our understanding of p53 as a mediator of developmental disease in addition to its role as a tumor suppressor.

Bruce A. Bowerman Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Appointed in 1989

Julianna Bozler Jane Coffin Childs Fellow

University of Pennsylvania

Appointed in 2019

Thomas J. Braciale Jane Coffin Childs Fellow

Australian National University, Australia

Appointed in 1976

Robert W. Brackenbury Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1975

J. Michael Bradshaw Jane Coffin Childs Fellow

Stanford University

Appointed in 2001

Colleen Brady Jane Coffin Childs - HHMI Fellow

Massachusetts General Hospital

Appointed in 2012

William A. Braell Jane Coffin Childs Fellow

Stanford University

Appointed in 1981

David G. Breckenridge Jane Coffin Childs Fellow

University of Colorado, Boulder

Appointed in 2003

Mark S.C. Bretscher Jane Coffin Childs Fellow

Stanford University

Appointed in 1964

Joshua Brickner Jane Coffin Childs Fellow

Stanford University

Appointed in 2020

Eve B. B. Briles Jane Coffin Childs Fellow

Washington University in St. Louis

Appointed in 1974

Hugh W. Brock Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1982

Nicholas Brown Jane Coffin Childs - HHMI Fellow

St. Jude Children's Hospital

Appointed in 2012

Breann Brown Jane Coffin Childs - Frederic M. Richards Fellow

Massachusetts Institute of Technology

Appointed in 2013

My primary research interest is studying the molecular basis of the diverse protein-protein interactions that underlie bacterial cell signaling. I am currently focusing on determining the various types of substrate interactions mediated by the E. coli Lon protease to understand how this critical regulator degrades certain proteins during cellular stress. Lon is one of the major proteases that mediates protein quality control via degradation of over half of the unfolded or misfolded proteins in the cell. Additionally, Lon degrades stably-folded regulatory proteins involved in response to several stresses such as DNA damage, heat shock, and oxidation. Using a combination of biophysical and biochemical assays, including electron microscopy, X- ray crystallography, analytical ultracentrifugation, and enzyme kinetics, my current goal is to identify the molecular interactions critical for Lon self-assembly and substrate recognition. With this detailed information, we can begin to understand in greater detail how Lon discriminates among various substrates to regulate critical cellular stress responses and survival.

Kathryn A. Brozek Jane Coffin Childs Fellow

University of Oregon

Appointed in 1991

Peter Bruno Jane Coffin Childs - HHMI Fellow

Brigham and Women's Hospital

Appointed in 2017

Senescence is an irreversible cell state characterized by permanent exit from the cell cycle that occurs in response to cellular stresses such as shortened telomeres and DNA damage. Thus, senescent cells accumulate as an organism ages and are thought to contribute to the gradual decline in tissue function as we age. Importantly, elimination of senescent cells in old mice extends healthy lifespan. Therefore, achieving a better understanding of the genetic underpinnings of senescence can lead to improved prevention and treatment of aging-related diseases._x000D_
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It is currently thought that senescence is mediated by three distinct pathways, characterized by their primary facilitators: p53, p16 and GATA4. However, there are likely many more factors that are critical to senescence induction. Thus, we conducted a whole genome CRISPR screen for genes necessary for replicative senescence in IMR90 primary fibroblasts. One novel gene identified was ZNF292. Thus, the objective of my postdoctoral work is to gain a more thorough understanding of the role of ZNF292 in senescence and tumorigenesis._x000D_
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James P. Bruzik Jane Coffin Childs Fellow

Harvard University

Appointed in 1991

Robert E. Bryant Jane Coffin Childs Fellow

Yale University

Appointed in 1973

Paula Bucko, Ph.D. Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2021

In response to DNA damage, the tumor suppressor protein p53 induces expression of stress-responsive genes to inhibit proliferation of cells with damaged DNA. Changes in p53 protein levels over time (p53 dynamics) impact cellular outcomes: p53 oscillations facilitate repair of DNA-damaged cells, whereas sustained levels of p53 promote senescence and cell death. While it is now established that p53 dynamics contribute to these competing cell-autonomous processes, how p53 dynamics regulate genes involved in non-cell-autonomous events, such as those involved in immune signaling, is not known. I propose to develop new tools and approaches to study the role of p53 in regulating immune gene expression in cancer cells and in mediating the killing of cancer cells by immune cells. This research will provide fundamental insights into the mechanisms that govern of cancer cell-immune cell interactions and pave the way for developing effective combination therapies to treat cancer

Ahmad I Bukhari Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 1971

Ahmad I Bukhari Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 1969

Alejandro Burga-Ramos Jane Coffin Childs - HHMI Fellow

University of California, Los Angeles

Appointed in 2013

Megan Burger Jane Coffin Childs - HHMI Fellow

Massachusetts Institute of Technology

Appointed in 2016

Daniel J. Burke Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1983

Debi P. Burma Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1956

Bruce F. Burnham Jane Coffin Childs Fellow

University of Oxford, England

Appointed in 1961

Janet L. Burton Jane Coffin Childs Fellow

Yale University

Appointed in 1997

Samuel E. Butcher Jane Coffin Childs Fellow

University of California, Los Angeles

Appointed in 1995

Matthew Cabeen Jane Coffin Childs - Merck Fellow

Harvard University

Appointed in 2011

David S. Cafiso Jane Coffin Childs Fellow

University of California, Berkeley /
Stanford University

Appointed in 1979

Cori Cahoon Jane Coffin Childs Fellow

University of Oregon, Eugene

Appointed in 2019

Sexually reproducing organisms faithfully transmit their genome to the next generation by forming haploid gametes, such as eggs and sperm. In contrast to oogenesis and other developmental processes, spermatogenesis is sensitive to small temperature changes, requiring a narrow isotherm of 2-7¬∫C below basal body temperature. Although failure to precisely thermoregulate spermatogenesis or exposure to elevated temperatures are strongly linked to both male infertility and an increased risk of testicular cancer, the mechanisms behind temperature-induced damage on male reproductive health remain unknown. Recent studies indicate that the composition and/or function of chromosome structures differ during oogenesis and spermatogenesis, which may contribute to the temperature-sensitivity of spermatogenesis. In Caenorhabditis elegans, we have found using structured illumination microscopy that the synaptonemal complex (SC), a meiosis specific structure central to the proper execution of key meiotic processes, is destabilized specifically in spermatocytes and not oocytes following heat-stress. My ongoing studies seek to understand the differences in SC organization and composition that render it temperature sensitive only in spermatogenesis. Overall, these studies will illuminate how temperature specifically affects genome integrity in developing sperm and identify the mechanisms that underlie temperature-associated infertility and cancer risk of the male germline.

Wei Wen Cai Jane Coffin Childs Fellow

Baylor College of Medicine

Appointed in 1997

Liang Cai Jane Coffin Childs Fellow

University of California, San Francisco /
Yale University

Appointed in 2008

Current Research: The role of actin cytoskeleton remodeling during epithelial morphogenesis.

Prior to coming to the United States in 2003, I received bachelor’s degree in science from Fudan University in Shanghai, China. My undergraduate thesis topic was characterization of bacteriophage T3 DNA ligase.¬î My graduate study was done under Dr. James E. Bear in the Department of Cell and Developmental Biology at the University of North Carolina, Chapel Hill. My dissertation title was “Coronin 1B coordinates actin dynamics in lamellipodia.¬î ¬†Currently, I am working with Dr. Keith Mostov in the Department of Anatomy at UCSF. ¬†I really enjoy the life of doing research, and am looking forward to continuing my scientific journey. In my free time, I like to hike and ski.”