Directory - Jane Coffin Childs Memorial Fund

Status

Year Appointed

Institution

Name

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Ron M. Prywes Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1985

Chinmay Purandare, Ph.D. Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2023

The hippocampus is a mental GPS that uses visual information to determine relative location. However, the neural pathways that convey visual information to the hippocampus are unknown. Dr. Chinmay Purandare will investigate this information transmission in Dr. Massimo Scanziani’s lab at the University of California, San Francisco. Dr. Purandare will use a novel set of visual cues, developed during his graduate studies, to directly activate hippocampal neurons and determine which visual brain regions are informing the hippocampus. Furthermore, Purandare would probe if the visual information conveyed is different depending on whether the subject is moving versus externally generated visual motion. Dr. Purandare’s research will further our understanding of circuit level connections between visual pathways and the hippocampus.

As a graduate student in Dr. Mayank Mehta’s lab at the University of California, Los Angeles, Purandare explored the minimal set of cues necessary for driving hippocampal responses. He developed novel visual stimuli and found that the hippocampus responds like sensory cortices when presented with these cues. This research led Dr. Purandare to the question of how these visual cues reach the hippocampus, which he will now explore in Dr. Scanziani’s lab.

Jen Quick-Cleveland Jane Coffin Childs Fellow

University of California, Santa Cruz

Appointed in 2018

RNA polymerase II (RNAPII) kinetics are well-known to influence splicing patterns. Recent evidence has revealed that many introns are spliced right after they are transcribed, opening the potential for cross-regulation between these two key processes. During transcription, RNAPII pauses during initiation and during 3’ end processing, and these pauses are thought to allow the recruitment of necessary protein factors. Although more transient, RNAPII also pauses throughout elongation, however the significance of these pauses is unclear. Importantly, many of these pauses occur near the exon-intron boundaries._x000D_
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I am working to uncover the mechanisms that govern co-transcriptional splicing decisions. I am investigating the impact of RNAPII pausing on changes in splicing patterns using a short artificial arrest sequence, which allows me to engineer RNAPII pauses in any location. This DNA element, combined with improved genome-wide approaches such as Single Molecule Intron Tracking (SMIT), will allow me to assess how RNAPII pauses impact splicing patterns in both yeast and human cells.

Ishwar Radhakrishnan Jane Coffin Childs Fellow

Scripps Research Institute

Appointed in 1995

Arun Radhakrishnan Jane Coffin Childs Fellow

University of Texas Southwestern Medical Center

Appointed in 2003

Miroslav Radman Jane Coffin Childs Fellow

Harvard University

Appointed in 1971

Stephanie Ragland Jane Coffin Childs Fellow

Boston Children's Hospital /
Harvard University Medical School

Appointed in 2019

A cornerstone concept of mammalian innate immunity is that our cells can detect bacteria and subsequently produce appropriate antibacterial responses. Bacterial detection is achieved through the action of protein receptors, called pattern recognition receptors (PRRs), that sense conserved bacterial molecules, termed pathogen-associated molecular patterns (PAMPs). Since the cellular localization of PRRs varies (e.g., cell surface, phagosomal lumen, cytosol), PRR and PAMP co-compartmentalization is required for bacterial detection. It therefore stands to reason that only bacteria that escape phagosomal confinement should have the capacity to stimulate cytosol-localized PRRs. In contrast, bacteria that cannot damage phagosomes will be confined (along with their PAMPs) to the phagosomal lumen, where they are only sensed by phagosome-localized PRRs. Despite this rationale, bacteria that are unable to escape from the phagosome (which is true for most bacteria studied to date) are somehow detected by cytosolic PRRs. I am studying how cytosolic PRRs gain access to phagosomal PAMPs, how phagosomal dynamics influence detection, how bacteria manipulate host-derived processes, and the consequences of bacterial detection on innate control of infection.

Tobias F.C. Ragoczy Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Appointed in 2001

Srinivasan Rajalakshmi Jane Coffin Childs Fellow

Yale University

Appointed in 1965

Alain Rambach Jane Coffin Childs Fellow

Stanford University

Appointed in 1975

Susannah Rankin Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1995

Sahana Rao, Ph.D. Jane Coffin Childs - HHMI Fellow

Broad Institute

Appointed in 2023

Oxidative phosphorylation is a central metabolic pathway that occurs within mitochondria. Decline in oxidative phosphorylation capacity is observed during aging and in many diseases. Dr. Sahana Rao aims to investigate how a tumor suppressor gene also suppresses mitochondrial biogenesis. Dr. Rao will also use a genome-wide screen to identify novel regulators of mitochondrial biogenesis. Rao will conduct these studies in Dr. Vamsi Mootha’s lab at the Broad Institute. Collectively, these studies will provide insight into the regulation of mitochondrial biogenesis. They may also inform on mitochondrial dysregulation in aged or diseased states.

As a graduate student in Dr. Daniel Bachovchin’s lab at Memorial Sloan Kettering Cancer Center, Rao investigated inflammasomes – innate immune sensors that detect pathogenic signals and form large signaling complexes to alert immune cells. Dr. Rao’s studies elucidated molecular mechanisms of the activation of two inflammasome proteins, NLRP1 and CARD8, and established new tools to activate inflammasomes. With her extensive training as a chemical biologist, Rao will now study cellular metabolism and mitochondrial biogenesis in her postdoc.

William C. Raschke Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Appointed in 1973

Jeffrey Rasmussen Jane Coffin Childs - Merck Fellow

University of California, Los Angeles

Appointed in 2013

My work in Alvaro Sagasti¬ís lab focuses on interactions between the epidermis and the axons of touch-sensing neurons. I am particularly interested in how the epidermis regulates axon repair following injury.

I grew up in Ithaca, NY and received my BS in Computational Biology from Brown University. During my graduate studies at University of Washington in Seattle, WA, I became interested in the remarkable and diverse behaviors of epithelial cells. For my thesis, I studied mechanisms of epithelial tube formation in C. elegans with Jim Priess at the Fred Hutchinson Cancer Research Center. The Priess lab was a great place to learn genetics and cell biology and I am currently applying this training to understand how our largest epithelial organ ¬ñ the skin ¬ñ regulates repair of the sensory nervous system. Outside of the lab, my wife and I enjoy exploring Los Angeles with our son.

David H. Raulet Jane Coffin Childs Fellow

University of Pennsylvania

Appointed in 1982

Elizabeth L. Read Jane Coffin Childs - Frederic M. Richards Fellow

Massachusetts Institute of Technology

Appointed in 2009

T cells recognize diverse molecular signatures of pathogens on the surfaces of infected or antigen-presenting cells, but a significant immune response is mounted against just a few of these signatures during a typical infection. I’m using mathematical models and computer simulations to study the mechanisms of this phenomenon, termed “immunodominance,¬î and its implications for viral infections, vaccine design, and autoimmunity.

I earned BAs in chemistry and mathematics from the University of Colorado at Boulder in 2003 and a PhD in physical chemistry from the University of California at Berkeley in 2008. ¬†Before I began working in Arup Chakraborty’s group at MIT, I studied light harvesting by photosynthetic plants and bacteria in the laser spectroscopy lab of Graham Fleming at Berkeley. This work inspired my interest in using theoretical and computational modeling to gain mechanistic understanding of complex biological systems. When not pursuing interdisciplinary science, I like to cook, run, swim, and read historical biographies.

Kirthi C. Reddy Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2005

Gregory T. Reeves Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2007

Louis F. Reichardt Jane Coffin Childs Fellow

University of Geneva, Switzerland /
Harvard University Medical School

Appointed in 1972

Louis F. Reichartdt Jane Coffin Childs Fellow

University of Geneva, Switzerland /
Yale University

Appointed in 1974

Marsha E. Reichman Jane Coffin Childs Fellow

Massachusetts Institute of Technology /
Harvard University Medical School

Appointed in 1974

Brian R. Reid Jane Coffin Childs Fellow

Harvard University Medical School /
Dartmouth Medical School

Appointed in 1964

John F. Reidhaar-Olson Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 1990

Kimberley Reinhold Jane Coffin Childs - HHMI Fellow

Harvard University Medical School

Appointed in 2017

Attila Remenyi Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2002

Hartmut C. Renger Jane Coffin Childs Fellow

New York University

Appointed in 1971

Alfred A Reszka Jane Coffin Childs Fund

University of Washington, Seattle

Appointed in 1992

Michel Revel Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 1963

Michael Rexach Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1993

Nicolas Reyes Jane Coffin Childs Fellow

Weill Medical College of Cornell University

Appointed in 2007

Hans O. Ribi Jane Coffin Childs Fellow

Stanford University

Appointed in 1987

Daniel Richard Jane Coffin Childs Fellow

Stanford University

Appointed in 2024

Aging is associated with decreased cognitive ability and enhanced risk of developing neurodegenerative diseases such as Parkinson’s and Alzheimer’s. The declining function of neural stem cells (NSCs) is partially responsible for these trends in the aging brain. While much is known about the genetics of late-stage neurodegenerative diseases, relatively little is known about changes that lead to the decline in NSC function.

Dr. Daniel Richard will investigate the accumulation of somatic mutations in NSCs in Dr. Anne Brunet’s lab at Stanford University. He will examine how these mutations change NSC gene expression and neuron production. Additionally, Dr. Richard will explore strategies to genetically manipulate somatic mutations to potentially enhance NSC function. Richard’s studies will provide much-needed insight into fundamental NSC biology during aging and may reveal novel therapeutic strategies for neurodegenerative diseases and cognitive decline.

Richard’s interest in the link between genetic changes and aging emerged from his graduate studies in Dr. Terence Capellini’s lab at Harvard University. There, Richard focused on the genetic regulation of knee development. By comparing functional regulatory regions in human and mouse fetal limbs, Richard discovered mutations associated with an increased risk for osteoarthritis later in life. Now, Richard will shift his focus to aging-related biological changes in NSCs and neurodegenerative diseases during his postdoctoral research.