Directory - Jane Coffin Childs Memorial Fund

Status

Year Appointed

Institution

Name

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Matthew Cabeen Jane Coffin Childs - Merck Fellow

Harvard University

Appointed in 2011

Bacterial biofilm regulation by D-amino acids

David S. Cafiso Jane Coffin Childs Fellow

University of California, Berkeley /
Stanford University

Appointed in 1979

Electrical properties of niological membranes

Emre Caglayan, Ph.D. HHMI-Jane Coffin Childs Fellow

Boston Children's Hospital, Harvard Medical School

Appointed in 2025

Uncovering oligodendrocyte lineage dynamics in the human brain using somatic mutations

Human brain development is challenging to study for many reasons. Dr. Emre Caglayan’s project as an HHMI-JCC Fellow aims to overcome experimental limitations related to studying brain development and provide unprecedented insight into how a brain develops over the human lifespan.

As a Ph.D. student in Dr. Genevieve Konopka’s lab at UT Southwestern Medical Center, Caglayan investigated human brain evolution. Using advanced genomics technologies, he found that human brains have unique functionalities used for the development and maturation of specialized cells relative to other closely related species.

Dr. Caglayan notes that the absence of non-invasive molecular tools has prevented further exploration of the human brain, and was captivated by the approach of Christopher Walsh’s lab to use somatic mutations as a “barcode” to trace cell lineages. This approach will enable Caglayan’s investigation into brain dynamics so that they can investigate how new mature oligodendrocytes are generated throughout a human lifespan. This research will provide fundamental insight into neurodevelopment and may reveal novel clues about how these processes go awry during neurodegeneration.

Cori Cahoon Jane Coffin Childs Fellow

University of Oregon, Eugene

Appointed in 2019

Defining mechanisms of heat-sensitive synaptonemal complex in spermatocytes

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

Genome-wide monitoring of genetic changes in cancer development

Liang Cai Jane Coffin Childs Fellow

University of California, San Francisco /
Yale University

Appointed in 2008

Actin cytoskeleton reorganization during tubulogenesis

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.”

Brendan Camellato, Ph.D. Jane Coffin Childs Fellow

Memorial Sloan Kettering Cancer Center

Appointed in 2025

Recording cell states and signaling events to reveal cell fate decisions during pancreatic islet differentiation

Gene transcription, the process of copying DNA into RNA for gene expression, is a complicated process that relies on sequences of DNA known as enhancers to help regulate the process. Enhancers are non-coding stretches of DNA that regulate the expression of a subset of genes.

Dr. Brendan Camellato made crucial insights into enhancer-mediated regulation during his thesis research in Dr. Jef Boeke’s lab at NYU Langone Health. In one of his projects, Camellato investigated transcriptional regulation across various species. In addition to being an impressive technical advance, this approach provided insight into a plausible mechanism for how genetic information is transferred and regulated in yeast and mouse embryonic stem cells.

Now, as a Fellow in Junhong Choi, Ph.D.’s lab at Memorial Sloan Kettering Cancer Center, Dr. Camellato will use enhancers as a tool to record cellular histories during normal development, and in diseased states. Using the recently developed ENhancer-based Genomic Recording of transcriptional Activity in Multiplex (ENGRAM), Camellato will investigate how cell signaling drives stem cell differentiation with single-cell resolution. His research promises to advance these important technologies, as well as provide unprecedented insight into human development.

John R. Cameron Jane Coffin Childs Fellow

Stanford University

Appointed in 1977

Chromosomal organization

Tod W. Campbell Jane Coffin Childs Fellow

Chemisches Institut der Universitat, Switzerland

Appointed in 1951

Carcinogenesis

Julie C. Canman Jane Coffin Childs Fellow

University of Oregon

Appointed in 2003

The mechanism of cytokinesis

Matthew Capek, Ph.D. Jane Coffin Childs Fellow

Harvard University

Appointed in 2026

Molecular mechanisms underlying ancient cross-kingdom interactions and terrestrial life

Matthew Capek, Ph.D. believes that by examining how organisms sense and respond to their closest neighbors we can deepen our understanding of basic biology while also gaining insight into human health, disease, and ecosystem stability. During his graduate research he uncovered the distinct ways through which flies sense and adapt to environmental temperatures. Now, as a Jane Coffin Childs Fellow, Capek will investigate the adaptation and cooperation between some of the first plant and animal pioneers to transition from living in the waters to living on land.

As a graduate student in Marco Gallio, Ph.D.’s lab at Northwestern University, Capek showed how responses to temperature evolved in fly species hailing from different environments, from temperate forests to hot deserts. Flies from mild climates avoid heat and have molecular differences in their receptors that directly sense temperature. Mojave Desert flies are instead attracted to heat, and this shift in behavior arises from a change in how the brain processes and interprets the signal. He also studied the cold-adapted fly Chionea alexandriana, showing that they generate heat in response to rapid cold challenges, carry molecular changes in pathways to cope with stress, and produce antifreeze proteins that prevent freezing in sub-zero temperatures.

For his fellowship in Nicholas Bellono’s lab at Harvard University, Capek will focus on understanding how interactions between mosses and springtails established the first terrestrial ecosystems. In water, moss sperm can swim to eggs to achieve fertilization, but life on land makes that journey far more difficult. Springtails help mosses reproduce on land by carrying sperm between moss sex organs. Capek will examine how mosses compel springtails to facilitate their reproduction, and determine what benefit motivates the springtails’ efforts. He predicts that understanding this ancient plant-animal cooperation will yield a new framework for understanding how molecular communication drives the evolution of complex life.

Bryce Carey Jane Coffin Childs - HHMI Fellow

Rockefeller University

Appointed in 2012

Metabolic connections to pluripotent chromatin

Philip L.M. Carl Jane Coffin Childs Fellow

King's College, London

Appointed in 1968

Viral and bacterial DNA

Marian B. Carlson Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1978

Regulation of sucrose utilization in yeast

Gordon G. Carmichael Jane Coffin Childs Fellow

Swiss Institute of Experimental Cancer Research, Switzerland

Appointed in 1975

Affinity chromatography

Lews Caro, Ph.D. HHMI-Jane Coffin Childs Fellow

University of Utah

Appointed in 2025

Evolution of receptor-ligand selectivity to evade bacterial ligand mimicry

Dr. Lews Caro is fascinated with the molecular arms race that occurs between a host and pathogen and how it shapes their evolution. Caro hypothesizes “that by understanding the molecular mechanisms of evolutionary phenomena, we can actually gain more insight into the evolutionary process itself.”

Caro’s graduate research in Michael Ailion’s lab at the University of Washington uncovered the mechanism of a toxin-antidote system in C. elegans. While such systems are widespread in bacteria and fungi, relatively few examples have been discovered in animals, and those few examples remain poorly characterized.

As a Fellow in Nels Elde’s lab at the University of Utah, Dr. Caro will explore the relationship between a special type of transmembrane protein, called ligand receptors, and the ligand itself. Pathogens secrete toxic ligand imitators which bind to host receptors and hijack normal host signaling. This exerts an evolutionary pressure on the receptor to escape activation by pathogen toxic ligands while retaining responsiveness to host ligands. Caro will use a combination of evolutionary analyses, functional and binding assays, and structural biology approaches to determine how receptors resolve this evolutionary conflict.

James M. Carothers Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2006

Controlling metabolic pathways with RNA aptamers

Agamemnon J. Carpousis Jane Coffin Childs Fellow

University of California, Santa Barbara

Appointed in 1983

Yeast centromere structure and function

Dana Carroll Jane Coffin Childs Fellow

Beatson Institute for Cancer Research, Scotland

Appointed in 1970

DNA template activity

Ava Carter Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2020

Zinc finger TFs in activity-dependent human neuronal gene regulation

Andrew P. Carter Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2003

Edward A. Carusi Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 1958

Chemical structure of RNA from tobacco mosaic virus

Pedro S. Carvalho Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2005

Molecular mechanisms to degrade abnoraml proteins

Jason M. Casolari Jane Coffin Childs Fellow

Stanford University School of Medicine

Appointed in 2006

Investigation of asymmetric RNA localization

Pau Castel Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2017

Novel effectors of oncogenic KRAS that regulate cell signaling

Joseph Castellano Jane Coffin Childs - Simons Foundation Fellow

Stanford University School of Medicine

Appointed in 2013

Effects of irradiation injury on systemic-neurogenic communication as targets for limiting cognitive dysfunction

During my Ph.D. studies at Washington University, I worked with David Holtzman to show that ApoE e4 may increase Alzheimer¬ís disease risk by impairing Ab clearance from the brain, thus shifting the onset of its accumulation. My interest in neurodegeneration and aging motivated me to understand factors that regulate aging and brain health in unconventional ways. My project as a Jane Coffin Childs fellow in Tony Wyss-Coray¬ís laboratory has been to elucidate a novel systemic-neurogenic communication mechanism that appears to be disrupted in the context of brain irradiation therapy. Specifically, I am investigating the role of immune signaling molecules in mediating the neurogenic and cognitive dysfunction observed in the post-irradiation syndrome in pediatric brain cancer patients. Additionally, I am actively pursuing whether related blood-borne signaling molecules in young plasma may be sufficient to ameliorate age-related decreases in cognition and synaptic plasticity. To examine these complex mechanisms, I am leveraging various physiological methods, including plasma transfer and parabiosis.

J. David Castle Jane Coffin Childs Fellow

Yale University /
University of California, Berkeley

Appointed in 1974

Release of secretory proteins

Kate Cavanaugh, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2021

Biophysical dissection of implantation defects resulting from maternal aging

Infertility represents a significant societal burden, as nearly 60% of human pregnancies fail before the embryo implants into the uterus. These miscarriages become more prevalent as women age above 35 years. But implantation remains a black box within development because it occurs within the mother’s body, so progress revealing its physical mechanisms is lagging. Early in preimplantation sages, primitive placental lineages must be specified for faithful implantation. Driving these lineage commitments are subcellular mechanical forces that transduce expression of downstream fate determinants for specification and ultimate invasion of placental tissues. However, in mammalian embryos of aged mothers, embryos display poor developmental health with decreased placental structures owing to impaired implantation. We hypothesize that these pathologies may stem from either early defects in tissue specification or later mechanical uterine invasion, both of which could give rise to age-related spontaneous abortions. This proposal therefore seeks to understand how the early cell biological and biophysical mechanisms are altered in the embryo with advanced maternal age, and how these mechanisms can be tuned to rejuvenate “aged” embryos to rescue developmental potential. Working in embryos of aged mice, we will combine approaches from cell and developmental biology, biophysics, and synthetic biology to ask: (1) Does maternal aging decouple the embryo’s upstream mechanics from downstream signal transduction during placental fate acquisition? (2) Is the logic of signal transduction for placental fate determinants altered via maternal aging? and (3) Do these age-related mechanisms together promote defective mechanical invasion during uterine implantation? Bridging these disparate scientific spheres will be critical in understanding infertility and improving female reproductive longevity.

Pelin M. Cayirlioglu Jane Coffin Childs Fellow

University of California, Los Angeles

Appointed in 2003

Genetic screen for regulators of neural connectivity

Carol L.M. Cech Jane Coffin Childs Fellow

Harvard University

Appointed in 1975

Constance L. Cepko Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1982

Developmental neurobiology

Heriberto D. Cerutti Jane Coffin Childs Fellow

Duke University

Appointed in 1992

Chlamydomonas genes in chloroplast DNA repair

QueeLim Ch'ng Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2001

Yunrong Chai Jane Coffin Childs Fellow

Harvard University

Appointed in 2006

Multicellularity in Bacillus subtilis

Debrabrata Chakravarti Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Appointed in 1994

Identification of putative retinoic acid cistrans isomerase

Glenn H. Chambliss Jane Coffin Childs Fellow

Universite de Paris, France

Appointed in 1971

Regulation of cellular differentiation in B. subtilis

Wendy C. Champness Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1982

Genetic control of cell lineage in c. elegans

David Chan Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 1996

Structural basis of membrane fusion in HIV infection

Phillip C. Chan Jane Coffin Childs Fellow

Insitut for Biochemie, Max-Planck-Institut

Appointed in 1959

Syntesis of steroids

Russell K. Chan Jane Coffin Childs Fellow

University of Washington, Seattle

Appointed in 1974

Vikram Chandra, Ph.D. Jane Coffin Childs Fellow

Harvard University

Appointed in 2021

The evolution of complex chemosensation

How animal brains evolved the capacity for sophisticated computation is not well understood. One major facet of this problem is the evolution of chemosensation. Chemosensation is the primary sense of most animals, and involves complex neural computations. We do not know how this sense evolved, or how most animals – which are aquatic invertebrates – perform chemosensation. I am studying chemosensation in an acoel worm, an aquatic invertebrate that by virtue of its phylogenetic position as the likely outgroup to all other animals with central nervous systems, retains some primitive features of early central nervous systems. Acoels nonetheless perform sophisticated behavior that requires complex chemosensory processing, but how their brains and chemosensors work is unknown. Using a combination of automated behavioral tracking, transgenics, and neural activity imaging, I aim to understand the logic of chemosensory processing in a tractable acoel worm. Through comparisons with known chemosensory mechanisms of other animals, this will shed light on how complex chemosensory systems evolved. This project will also establish experimental approaches for the future study of neural computations and behavior in acoel worms and other aquatic invertebrates.