Directory - Jane Coffin Childs Memorial Fund

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Joshua Meisel Jane Coffin Childs - Merck Fellow

Massachusetts General Hospital

Appointed in 2017

Molecular oxygen presents a fundamental biological problem: it is vital for life, yet also incredibly toxic. As the terminal electron acceptor in aerobic respiration and the redox engine of mitochondria, oxygen provides eukaryotes with the vast majority of their energy. However when molecular oxygen is reduced it can form damaging reactive species, and recent work has demonstrated that animals with genetic lesions in the mitochondrial respiratory chain are extremely vulnerable to oxygen toxicity. How animals have evolved to manage this double-edged sword remains a fundamental question._x000D_
The biology and natural ecology of the nematode C. elegans make it an attractive system in which to study oxygen tolerance. Wild type C. elegans are tolerant of oxygen concentrations ranging from 1% to 100%, and years of genetic studies have generated a rich toolbox of mitochondrial mutants. I will use these mutants to study the biology of oxygen tolerance, which may simultaneously shed light on the connection between mitochondrial disease and oxygen toxicity.

Justine A. Melo Jane Coffin Childs Fellow

Massachusetts General Hospital

Appointed in 2005

Elija Mena Jane Coffin Childs - HHMI Fellow

Brigham and Women's Hospital

Appointed in 2020

Ubiquitylation is a post-translational modification that regulates the stability of thousands of proteins in our cells. The specificity for ubiquitylation is typically conferred by E3 ubiquitin ligases that attach ubiquitin onto substrate proteins. Despite the critical role that ubiquitylation plays in regulating the abundance and activity of many proteins, most ubiquitylation pathways are still poorly understood and many of the estimated ~600 E3 ubiquitin ligases have no known protein substrates.

Our lab has developed the Global Protein Stability (GPS) assay, which is a way to rapidly monitor protein stability using fluorescent proteins. We have recently been adapting this approach for library-on-library genetic screens in order to map, in parallel, dozens of ubiquitylation substrates to their cognate E3 ubiquitin ligases. We have also been using GPS screens to find degradation pathways specific to particular intracellular compartments. Together, these approaches will shed light on ubiquitylation pathways that are important for human health.

Mortimer L. Mendelsohn Jane Coffin Childs Fellow

University of Cambridge, England

Appointed in 1957

Michael D. Mendenhall Jane Coffin Childs Fellow

University of California, Santa Barbara /
Scripps Research Institute

Appointed in 1985

Carlos Mendez-Dorantes, Ph.D. Jane Coffin Childs Fellow

Dana-Farber Cancer Institute

Appointed in 2021

Long interspersed element-1 (LINE-1) is the only active, protein-coding transposon in humans. LINE-1 overexpression and LINE-1 retrotransposition are hallmarks of human cancers, although the impact of LINE-1 activity on cancer genomes and cancer cell growth remains poorly understood. My research focuses on addressing the hypothesis that LINE-1 retrotransposition causes substantial gross genome instability in cancers. Supporting this hypothesis, a recent pan-cancer analysis demonstrated associations between somatically-acquired LINE-1 insertions and segmental copy-number changes. Moreover, our lab recently identified that the Fanconi anemia/ BRCA pathway is required for growth of LINE-1(+) cells, suggesting that this DNA repair pathway might limit genotoxic effects of LINE-1. I am developing several approaches to assess the impact of LINE-1 on genome integrity, and I am evaluating the contribution of the FA/ BRCA pathway to LINE-1-associated DNA damage. These studies will be the first to evaluate the scope of LINE-1-mediated genome instability and should inform efforts to exploit LINE-1 genotoxicity as a cancer therapeutic strategy.

Florian T. Merkle Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2008

The sleep disorder narcolepsy is caused by the degeneration of hypocretin neurons. The goal of my research is to derive hypocretin neurons from narcoleptic patients to study the cause of hypocretin neuron loss.

I was born in Konstanz, Germany and moved to Minnesota at an early age. As a teenager, I decided I wanted to become a neurosurgeon and spent my summers in a neurosurgery laboratory. I discovered I preferred working at the bench and, as an undergraduate at Caltech, I explored different fields of neuroscience. I was most fascinated by the problem of how the brain develops, and studied the lineage and organization of neural stem cells and their progeny in the postnatal brain. My current work combines my interests in cell type specification, the connection of circuitry to behavior, and developing in-vitro models of human diseases. In my free time, I enjoy hiking, cycling, cooking, and bartending.

John P. Merlie Jane Coffin Childs Fellow

Institut Pasteur, France

Appointed in 1973

Janet E. Mertz Jane Coffin Childs Fellow

Stanford University /
MRC Center, University Medical School, UK

Appointed in 1973

Kailin Mesa Jane Coffin Childs - HHMI Fellow

New York University

Appointed in 2017

Several vertebrate species have the astonishing ability to regenerate their limbs following amputation. In mammals, including both mice and humans, this regenerative capability has been restricted to the digit tip. Both digit tip and complete limb regeneration follow a stereotypic process termed epimorphic regeneration where a population of progenitor cells, termed the blastema, form at the injury site to replace the multiple tissues lost (including blood vessels, nerves, bone, etc.). Several studies have demonstrated that macrophages are essential for epimorphic regeneration. However, it remains largely unknown how macrophages facilitate blastema rather than scar formation. Utilizing the mouse digit tip, which displays regenerative or scarring outcomes dependent on amputation site, we are functionally testing which immune cell types uniquely contribute to epimorphic regeneration. Furthermore, by combining diverse genetic tools with intravital imaging, we are beginning to understand how injury-induced inflammation yields a permissive tissue environment for epimorphic regeneration in mammals.

David G. Mets Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2009

Tycho Mevissen Jane Coffin Childs - HHMI Fellow

Harvard University Medical School

Appointed in 2017

DNA interstrand cross-links (ICLs) covalently connect the two strands of DNA, thereby blocking essential processes including DNA replication and transcription. Cells have evolved intricate pathways to repair ICLs and other DNA lesions to ensure genome integrity. In the Walter laboratory, we use egg extracts from the African clawed frog Xenopus laevis to biochemically dissect the molecular events during DNA replication and repair. Importantly, these and other processes are faithfully recapitulated in this highly tractable cell-free system._x000D_
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My current work focuses on how different lesions, including ICLs, are repaired in a transcription-dependent manner. Although Xenopus egg extracts are generally considered to be transcriptionally quiescent, I set out to develop an in vitro transcription system to eventually investigate transcription-coupled DNA repair pathways of chemically distinct lesions. My study aims to biochemically characterize the underlying mechanisms as well as to identify novel factors involved in transcription-coupled DNA repair._x000D_

Elliot M. Meyerowitz Jane Coffin Childs Fellow

Stanford University

Appointed in 1977

Yuxuan Miao Jane Coffin Childs Fellow

Rockefeller University

Appointed in 2016

My research interest is to harness the power of immune system to combat cancer. This goal requires sophisticated understanding in both immunology and cancer biology. My prior graduate training has equipped me with extensive knowledge in immunology, and showed me how the immune system evokes robust and multilayered responses to defend our body against infections. However, compared to the vigorous response to infections, the immune system often becomes incompetent when it encounters cancer, especially malignant tumors. My goal during the fellowship period is to develop a cancer model in which I can trace the co-evolution between tumor-initiating stem cells and immune system, ultimately to the point of evasion of immune surveillance, so that I can identify the root of the blunted ant-tumor immune response during the cancer progression. With Dr. Fuchs’ expertise in epithelial stem cells and cancers, and my background in immunology, I feel that I’m uniquely poised to tackle this fascinating problem.

Roger L. Miesfeld Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1983

Peter J. Mikulecky Jane Coffin Childs Fellow

Scripps Research Institute

Appointed in 2006

Marcos E. Milla Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1990

Allan M. Miller Jane Coffin Childs Fellow

Harvard University

Appointed in 1986

Stephen C. Miller Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1998

Elizabeth A. Miller Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2000

Craig T. Miller Jane Coffin Childs Fellow

Stanford University School of Medicine

Appointed in 2002

Caroline Mirzayan Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 1993

Nawin C. Mishra Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1967

Prashant Mishra Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2010

I am investigating mechanisms of mitochondrial fusion within cells. The goal is to gain a better understanding of how mitochondrial dynamics are regulated.

My interest in scientific research began when I was young, and was fostered through participation in research programs and science fairs in junior high and high school. ¬†After completing my bachelor’s degree in biochemical sciences at Harvard University, I worked briefly for a biotechnology company developing treatments for patients suffering from rare genetic disorders. ¬†I then entered an MD/PhD program the University of Texas Southwestern Medical Center, allowing me to conduct basic science research while receiving training in patient care. ¬†I currently conduct research as a postdoctoral fellow at the California Institute of Technology, and plan to establish my own basic science laboratory in the future.

Kevin J. Mitchell Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1998

Patrick Mitchell Jane Coffin Childs - Simons Foundation Fellow

University of California, Berkeley

Appointed in 2016

Shekhar Mitra Jane Coffin Childs Fellow

Yale University

Appointed in 1981

Rachel M. Mitton-Fry Jane Coffin Childs Fellow

Yale University

Appointed in 2004

Satoru Miura Jane Coffin Childs - Genentech Fellow

University of California, San Diego

Appointed in 2015

Hideo Miyawaki Jane Coffin Childs Fellow

Yale University

Appointed in 1963

Joshua Modell Jane Coffin Childs - Simons Foundation Fellow

Rockefeller University

Appointed in 2014

Erica Moehle Jane Coffin Childs - Simons Foundation Fellow

University of California, Berkeley

Appointed in 2015

Just like people, cells have to deal with stress. I study how stressed cellular organelles such as mitochondria communicate with the nucleus, and how this stress response is coordinated in normal settings and dysregulated in disease._x000D_
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I studied genetics as an undergraduate at the University of California, Berkeley, and then worked at Sangamo BioSciences to help develop human genome editing with engineered nucleases. I was then an NSF Fellow in the Tetrad PhD program at the University of California, San Francisco, where I worked in Christine Guthries laboratory. There, I studied how pre-mRNA splicing is regulated in particular, how the cell coordinates a pre-mRNAs transcription and its splicing. My interest in how discrete molecular processes are integrated inside the cell continues during my postdoctoral fellowship in Andrew Dillins laboratory, where I am studying a remarkable pathway called the mitochondrial unfolded protein response. In this pathway, nuclear-encoded mitochondrial protein chaperones are upregulated in response to signals from mitochondria experiencing proteotoxic stress. I am using a disease-in-a-dish model that combines human stem cell technology with genome editing approaches.

Karen E. Moore Jane Coffin Childs Fellow

University of Oregon

Appointed in 1988

Michael Moore Jane Coffin Childs Fellow

Rockefeller University

Appointed in 2011

Jeffrey Moore Jane Coffin Childs - HHMI Fellow

Harvard University

Appointed in 2015

My research investigates the neural circuits that control instinctive behavior. Previously, my work focused on the innate active sensing behaviors of rodents that dominate exploration and social interactions. This work has led me to focus on questions that involve the nature of the motivational and descending drives that enable animals to generate robust and instinctive motor patterns in the appropriate context. With the expertise of the Dulac Laboratory, I hope to provide insight into these questions by defining the roles of specific, molecularly-defined cell types and neuronal circuit connectivity patterns that relate to such control. I hope to provide a unique perspective that stems from a background in engineering and the neural control of movement.

Jeffrey Morgan Jane Coffin Childs - HHMI Fellow

University of Utah

Appointed in 2019

The ability of cells and organisms to sense and respond to change is fundamentally driven by dynamic interactions between many different types of molecules. Although we understand some of these interactions, there are many to be uncovered.

I am investigating the landscape of RNA-metabolite interactions and their role in gene regulation. Although RNAs and small molecules can form specific and high-affinity interactions, we know effectively nothing of the RNA-metabolite interactome that might be present in eukaryotic cells. Using RNA-structure probing technologies coupled with high-throughput sequencing, I am studying a broad pool of human RNAs in various metabolic contexts, which will uncover the scope of interactions between human RNAs and human metabolites, identify the specific RNA-metabolite interactions that do occur, and allow us to test the role of these interactions in gene regulation. In complement to this approach, we have developed a screening platform to simultaneously measure the affinity between specific RNAs and 450+ human metabolites. This platform has allowed for rapid, targeted screening of viral RNAs that might sense host metabolism via RNA-metabolite interactions and can be applied to any RNA of interest.

Gregg B. Morin Jane Coffin Childs Fellow

Yale University

Appointed in 1988

Roger J. Morris Jane Coffin Childs Fellow

University of Connecticut Health Center

Appointed in 1975

Frank Moss Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2019

Walther H. Mothes Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1998

Sherry L. Mowbray Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1983

J. Brian Mudd Jane Coffin Childs Fellow

University of California, Davis

Appointed in 1958

Sabin Mulepati Jane Coffin Childs - HHMI Fellow

Harvard University

Appointed in 2015

I received my BS in Biochemistry from Susquehanna University and my Ph.D. in molecular biophysics in Professor Scott Baileys lab at Johns Hopkins University. Broadly speaking, I am interested in exploring the structure-function relationship of biological macromolecules. For my Ph.D. thesis, I used different structural and biochemical methods to investigate the mechanism by which bacteria use their CRISPR immune system to destroy foreign DNA._x000D_
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In my postdoc with Professor Sunney Xie at Harvard University, my research focuses on the effects of chromatin structure on eukaryotic gene expression. More specifically, I am interested in understanding the dynamics of DNA supercoiling at a single-cell level. Outside the lab, I enjoy playing soccer and going on hikes.