Directory - Jane Coffin Childs Memorial Fund

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Rebecca M. Pruss, Ph.D. Jane Coffin Childs Fellow

University College

Project Title: Schwann cells in peripheral nervous systems interactions

Ron M. Prywes, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Growth factor regulation of transcription studied in vitro

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

University of California, San Francisco

Project Title: Transmission of visual information from the retina to the hippocampus

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 E. Quick-Cleveland, Ph.D. Jane Coffin Childs Fellow

University of California, Santa Cruz

Project Title: The impact of RNA polymerase II pausing on co-transcriptional splicing

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, Ph.D. Jane Coffin Childs Fellow

Scripps Research Institute

Project Title: NMR studies of the phosphoCREB-CBP interaction

Arun Radhakrishnan, Ph.D. Jane Coffin Childs Fellow

University of Texas Southwestern

Project Title: Biophysical studies of SCAP, a cholesterol sensor

Miroslav Radman, Ph.D. Jane Coffin Childs Fellow

Harvard University

Project Title: DNA in genetic recombination

Stephanie Ragland, Ph.D. Jane Coffin Childs Fellow

Boston Children's Hospital /
Harvard University Medical School

Project Title: Mechanisms of transport for bacterial molecules across phagosomal membranes

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 FC. Ragoczy, Ph.D. Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Project Title: Chromatin conformation at the human beta-globin locus

Srinivasan Rajalakshmi, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Regulation of purines and pyrimidines

Rohith Rajasekaran, Ph.D. Robertson Foundation-Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Reprogramming STAT signaling using engineered fusion proteins to tune CAR T cell antitumor activity.

Rohith Rajasekaran, Ph.D., wants to study how naturally evolved molecular systems can be redesigned to program new cellular behaviors. Rajasekaran’s previous research repurposed a bacterial positioning system to turn mammalian cells into “two-way radios” that can send and receive biological information. Now, as a Robertson Foundation – Jane Coffin Childs Fellow, Rajasekaran will rewire T cell signaling in modular, tunable ways to improve their efficacy, durability, and safety in cancer immunotherapies.

Rajasekaran’s thesis research in Scott Coyle’s lab at the University of Wisconsin—Madison ported two bacterial proteins (MinD and MinE) into mammalian cells. MinD and MinE are normally involved in establishing bacterial polarity, but Rajasekaran repurposed them to control and pattern intracellular mammalian biology. He used them to track signaling (like kinase activity) and to organize processes such as condensate formation and actin filament growth. He also built genetic circuits that linked natural cellular processes to MinD/MinE signaling patterns, allowing those signaling “rhythms” (frequency and strength) to serve as a readout of cellular activity, revealing when genes turn on, how proteins are broken down, and how stem cells develop into different cell types.

In Kole Roybal’s lab at UCSF, Rajasekaran will apply similar ideas to chimeric antigen receptor (CAR) T cell therapies. CAR T cancer therapies have shown great promise yet are only effective for a subset of patients and have limited duration for responding patients. Rajasekaran will build on the Roybal Lab’s finding that oncogenic fusion genes enhance CAR T therapies, he will design synthetic fusion proteins that adjust the strength and timing of key signaling pathways in T cells. By linking signaling patterns to T cell behavior, he aims to create better, longer lasting, and safer CAR T therapies for more patients.

Alain Rambach, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Genetics of eukaryotic DNA

Susannah Rankin, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: The surface contraction waves of Xenopus eggs reflect cell cycle state

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

Broad Institute

Project Title: Post-transcriptional regulation of mitochondrial biogenesis

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, Ph.D. Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Project Title: Generation of antibody diversity

Jeffrey P. Rasmussen, Ph.D. Jane Coffin Childs - Merck Fellow

University of California, Los Angeles

Project Title: Interactions between sensory neurons and skin

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, Ph.D. Jane Coffin Childs Fellow

University of Pennsylvania

Project Title: Genetics restrictions in cytotoxic T cell induction

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

Massachusetts Institute of Technology

Project Title: Understanding the origin of immunodominance in mouse models and humans with diverse host genetics

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, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Genetic analysis of innate immunity in C. elegans

Gregory T. Reeves, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Spatial regulation of the NF-kappaB pathway in Drosophila embryogenesis

Louis F. F.. Reichardt, Ph.D. Jane Coffin Childs Fellow

University of Geneva, Switzerland /
Harvard University Medical School

Project Title:

Louis F. Reichardt, Ph.D. Jane Coffin Childs Fellow

University of Geneva /
Yale University

Project Title: Binding of bacteriophage lambda with host DNA

Marsha E. Reichman, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology /
Harvard University Medical School

Project Title: Fetal cell surface antigens of BALB/c mice

Brian R. Reid, Ph.D. Jane Coffin Childs Fellow

Dartmouth Medical School /
Dartmouth Medical School

Project Title: Mechanisms of RNA interaction in protein synthesis

John F. Reidhaar-Olson, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Specificity and flexibility in a-lytic-protease

Kimberly Reinhold, Ph.D. Jane Coffin Childs - HHMI Fellow

Harvard Medical School

Project Title: The neural substrate of learned habits

Attila Remenyi, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Structure of MAP-kinase signaling modules

Hartmut C. Renger, M.D., Ph.D. Jane Coffin Childs Fellow

New York University

Project Title: Temperature-sensitive transformation mutant of SV40 virus

Alfred A. Reszka, Ph.D. Jane Coffin Childs Fund

University of Seattle, Washington

Project Title: Cytoskeleton of phosphatase detransformed cells

Michel Revel, M.D., Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Nucleic acid chemistry

Michael Rexach, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Molecular dissection of nuclear protein import

Nicolas Reyes, Ph.D. Jane Coffin Childs Fellow

Weill Medical College of Cornell University

Project Title: Conformational changes of the glutamate transporter accompanying the release of ligands to the cytoplasm

Matthew J. Reynolds, Ph.D. Jane Coffin Childs Fellow

Washington University in St. Louis

Project Title: Structural mechanisms for higher-order microtubule assembly function in parasites

Dr. Matthew Reynolds is fascinated with the elegant structures of our cytoskeleton – a large network consisting of protein fibers and associated proteins that gives shape and structure to cells. During his thesis research he developed machine-learning based techniques to enable the structural determination of curved and bundled actin structures. In his fellowship, Reynolds will detail specialized cytoskeleton super-assemblies from parasitic cells.

During Reynolds’ thesis research in Dr. Greg Alushin’s lab at Rockefeller University, he made important contributions to processes involved in cryo-EM structure determination. Reynolds developed computational techniques that were crucial in reconstructing bent F-actin segments and bundled F-actin that help shape and move cells.

Now, in Dr. Rui Zhang’s lab at Washington University in St. Louis, Reynolds will apply his structural biology expertise to more complex cellular systems. He will continue to investigate the cytoskeleton and will use a combination of cryo-EM and cryo-electron tomography (cryo-ET) to examine microscopic single-cell organisms. These studies will provide mechanistic insights into the nanoscale protein-protein interactions that drive micron-scale cytoskeleton organization in single-celled parasites. His research will likely push forward technological development in structural determination via cryo-EM and cryo-ET. Reynolds anticipates that his findings will inform parasitic disease models and may reveal novel therapeutic targets.

Hans O. Ribi, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: MCH-antigen complex and helper T-cell activation

Daniel J. Richard, Ph.D Jane Coffin Childs Fellow

Stanford University

Project Title: Decoding Aging Neurogenic Niches: Unraveling Somatic Mutations, Clonal Dynamics, and Functional Decline

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.