Directory - Jane Coffin Childs Memorial Fund

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Year Appointed

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Phi Nguyen, Ph.D. Jane Coffin Childs Fellow

Columbia University /
New York State Psychiatric

Appointed in 2022

Major depressive disorder (MDD) is a psychiatric disorder with a lifetime prevalence of ~15% and is the leading cause of disability worldwide¹. The societal burden of MDD is immense, causing profound personal suffering and economic loss, which has recently been intensified by the Covid-19 pandemic². The most effective treatments for MDD, a class of antidepressants called the selective serotonin reuptake inhibitors (SSRIs), are successful in achieving remission, but only in ~40% of patients³. Despite being in use for over 50 years, it remains unknown how SSRIs modulate neural circuit function in patients that achieve remission and where these mechanisms are disrupted in those that do not. Thus, a fundamental question remains: What are cellular and molecular mechanisms that mediate antidepressant response and resistance? Defining the answers to this question could provide fundamental insights into the pathophysiology of MDD and uncover novel substrates for future precision medicine approaches.

Shiro Nii Jane Coffin Childs Fellow

Columbia University

Appointed in 1966

Maho Niwa Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1994

Steven K. Nordeen Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1978

Yitzhak Norman, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2022

Speech is a defining characteristic of human cognition. It provides humans with the flexibility to convey an unlimited range of thoughts and feelings using a limited number of basic elements. Over the past decade, intracranial electrocorticography (ECOG) recordings in patients have provided invaluable insights into the neural mechanisms underlying speech perception and production. While significant progress has been made, basic questions still remain regarding the functional architecture of the neuronal circuits involved. Particularly, we do not know how the brain assembles phonemes into words, and words into meaningful goal-directed utterances. Such phonemic-to-semantic transformation relies on real-time interactions between the speech cortex and distributed memory networks that encode, store, and retrieve our lexical and semantic knowledge quickly and efficiently. The hippocampus, as a critical node in this declarative memory system, is believed to play a key role in coordinating such processes in real time.

My research seeks to elucidate the cortical-hippocampal interaction during speech perception and production, and more broadly, to unravel the interface between speech representations and long-term memory. To accomplish this, I combine ECOG recordings with 7T fMRI to measure neuronal activity simultaneously from the hippocampus and speech cortex during perception and production of speech.

Dominic P. Norris Jane Coffin Childs Fellow

Harvard University

Appointed in 1995

Abraham Novogrodsky Jane Coffin Childs Fellow

Albert Einstein College of Medicine

Appointed in 1964

Roni Nowarski Jane Coffin Childs Fellow

Yale University

Appointed in 2012

Kathaleen O'Connor-Giles Jane Coffin Childs Fellow

University of Wisconsin, Madison

Appointed in 2004

Patrick H. O'Farrell Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1974

Elizabeth M. O'Neill Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1995

Charles E.Y. Oh Jane Coffin Childs Fellow

University of California, San Francisco /
California Institute of Technology

Appointed in 1988

Eugene Oh Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2013

Ubiquitylation is a versatile post-translational modification required for most cell fate decisions. During neurogenesis, ubiquitin-dependent mechanisms ensure the irreversible transformation of neural stem cells into neurons. By contrast, the misregulation of the ubiquitylation system can set off a wide range of developmental abnormalities, from uncontrolled cell proliferation and tumor formation to neurodegeneration and cell death. Despite its medical relevance, our understanding of how ubiquitylation governs the course of human neurogenesis is far from complete. For my research fellowship, I propose to develop a large-scale screening platform to identify the ubiquitylating enzymes that promote the maintenance of undifferentiated human stem cells as well as those that facilitate the specification of neural cell fates. To better grasp the physiological parameters that underlie the directionality of cellular differentiation, I will define the collection of endogenous substrate proteins modified by the newly identified enzymes. Aside from generating a list of substrates, I aim to study the functional consequences of ubiquitylation by characterizing substrate mutants that are resistant to ubiquitylation in stem cells. Together, my results will shed light on fundamental principles of human development and potential mechanisms that cause neuronal cancers and neurodegenerative disorders.

Melanie Ohi Jane Coffin Childs Fellow - Agouron

Harvard University Medical School

Appointed in 2002

Hiroto Okayama Jane Coffin Childs Fellow

Stanford University

Appointed in 1978

James T. Olesen Jane Coffin Childs Fellow

Harvard University

Appointed in 1990

Brian C.M. Oliver Jane Coffin Childs Fellow

Stanford University

Appointed in 1988

Kassandra Ori-McKenney Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2011

Joseph Orly Jane Coffin Childs Fellow

University of California, San Diego

Appointed in 1978

Stephen I. Oroszlan Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1963

Jose Orozco, M.D.,Ph.D. Jane Coffin Childs Fellow

Dana-Farber Cancer Institute

Appointed in 2023

Organisms adapt to scarce and bountiful nutrient environments by employing nutrient signaling pathways. Sugar is a rich source of energy and carbon for organisms, Dr. Jose Orozco will explore sugar-sensing pathways using biochemical and genetic approaches to discover sugar-regulated kinases and their roles in metabolic adaptation. Dr. Orozco will conduct his work in Dr. Lewis Cantley’s lab at Dana-Farber Cancer Institute. These studies may reveal a new therapeutic target to alleviate metabolic maladaptive responses to the chronic overconsumption of sugars and carbohydrates.

As a graduate student in Dr. David Sabatini’s lab at Massachusetts Institute of Technology, Orozco investigated the nutrient-regulated pathway that controls the target of rapamycin complex 1 (mTORC1) kinase. Specifically, Dr. Orozco discovered a new amino acid sensor that integrates S-adenosylmethionine levels, identified a metabolic product of glycolysis that communicates with mTORC1, and discovered new genes in the mTORC1 pathway. Dr. Orozco will continue pursuing his interests in the link between metabolism and signal transduction pathways in his investigations of MondoA.

Terry L. Orr-Weaver Jane Coffin Childs Fellow

Carnegie Institute for Science

Appointed in 1984

Lev Z. Osherovich Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2003

Jessica Osterhout Jane Coffin Childs - HHMI Fellow

Harvard University

Appointed in 2016

Thermoregulation is fundamental for survival; even slight changes in body temperature have a dramatic effect on vital processes such as sleep, appetite, and thirst, and during an immune response, febrile patients often become fatigued, antisocial, and exhibit other sickness-related behaviors. Specific brain areas are thought to control body temperature by triggering various mechanisms that produce or dissipate heat, but how thermoregulatory neurons modulate thermo-adaptive and other behaviors is unknown. I will use recently developed tools for genetic profiling and circuit analysis to molecularly identify thermoregulatory and fever-inducing neurons and map their connectivity patterns, thereby gaining new insight into thermoregulatory circuits and how they are connected to other homeostatic and social functions in the brain.

Paul Ottolenghi Jane Coffin Childs Fellow

Carlsberg Laboratories, Denmark

Appointed in 1957

Youcef Ouadah Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2019

Adegboyega (Yomi) Oyelere Jane Coffin Childs Fellow

Yale University

Appointed in 1998

Carol O. Pabo Jane Coffin Childs Fellow

Harvard University

Appointed in 1980

Fredieric Pacques Jane Coffin Childs Fellow

Brandeis University

Appointed in 1996

Jon Paczkowski Jane Coffin Childs Fellow

Princeton University

Appointed in 2015

Quorum sensing is a mechanism of cell-cell communication that allows bacteria to synchronously control processes that are only productive when undertaken in unison by the collective. I will focus on Pseudomonas aeruginosa because it has a well-defined quorum sensing network that is essential for biofilm formation and virulence factor production, and because P. aeruginosa is an important pathogen that affects cystic fibrosis sufferers, cancer patients undergoing chemotherapy, burn victims, and patients with implanted medical devices._x000D_
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My work combines structural biology, chemistry, and genetics to define the mechanisms underlying activation and inhibition of quorum-sensing receptors with the aim of understanding how quorum sensing receptors accurately decode the information contained in small molecule signals to drive collective behaviors. These investigations could lead to strategies for controlling quorum sensing, potentially resulting in the development of anti-microbial drugs aimed at bacteria that use quorum sensing to control virulence and biofilm formation.

Andrea W. Page-McCaw Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1998

Athma Pai Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2013

Alexander F. Palazzo Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2004

Michael J. Palladino Jane Coffin Childs Fellow

University of Wisconsin, Madison

Appointed in 2001

Vito J. Palombella Jane Coffin Childs Fellow

Harvard University

Appointed in 1989

Duojia Pan Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1993

Jie Pan Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1999

Xingjie Pan, Ph.D. Jane Coffin Childs - HHMI Fellow

Harvard University

Appointed in 2022

During mammalian development, coordinated cell differentiation and migration convert a simple neural tube into a brain with more than a hundred anatomical regions and probably more than a thousand cell types. How do these cell types emerge? How do cells migrate to their destined locations? How do cells communicate with each other? These are some fundamental problems in brain development.

As a postdoctoral fellow in Xiaowei Zhuang’s lab at Harvard, I develop new methods to systematically study these problems in mouse brain development. I develop new computational methods to connect cells from MERFISH spatial transcriptomics measurements into trajectories and determine cell-cell communication pathways activated in each cell. The reconstructed trajectories will allow me to comprehensively map the differentiation, maturation, and migration of individual cells. I will identify which cell-cell communication pathways are functionally crucial for generating each cell type. Then I will develop high throughput imaging-based screen methods to validate the discoveries.

Niranjan B. Pandey Jane Coffin Childs Fellow

Harvard University /
Massachusetts Institute of Technology

Appointed in 1991

Scott R. Panzer Jane Coffin Childs Fellow

Yale University

Appointed in 1994

Claude A. Paoletti Jane Coffin Childs Fellow

Stanford University

Appointed in 1968

William N. Pappano Jane Coffin Childs Fellow

Johns Hopkins University

Appointed in 2004

Sang-Hyun Park Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2000

Eunyong Park Jane Coffin Childs - HHMI Fellow

Rockefeller University

Appointed in 2013

My current research focus is on understanding molecular mechanisms of CLC proteins, ubiquitous membrane proteins that transport chloride ions across membranes. The CLC proteins are involved in various biological processes including regulation of membrane potential, electrolyte/fluid transport across epithelia, and control of intravesicular pH. Mutations in CLC genes cause many hereditary disorders in humans. An interesting aspect of the CLC family is that a common structural architecture seems to be used for both active and passive ion transport. Some CLCs are chloride channels, which provide a passive pore for chloride ion conduction, whereas others function as secondary active transporters that exchange two chloride ions for one proton. Despite recent advances in our understanding of their mechanisms, fundamental questions remain unanswered, especially regarding how exactly CLC transporters couple the transfer of chloride and proton ions and what leads to the mechanistic difference between the channels and transporters. In the MacKinnon lab, I use structural and functional approaches to address these questions.