Directory - Jane Coffin Childs Memorial Fund

Status

Year Appointed

Institution

Name

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Mina Kojima Jane Coffin Childs Fellow

Yale University

Appointed in 2019

Dissecting the molecular mechanisms that trigger zygotic genome activation

Prasanna R. Kolatkar Jane Coffin Childs Fellow

Purdue University

Appointed in 1992

Virus receptor interactions on a molecular level

Anthony Koleske Jane Coffin Childs Fellow

Whitehead Institute /
Massachusetts Institute of Technology

Appointed in 1994

A loss of caveolae/caveolin in transformed cells

Suzanne F. Komili Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Appointed in 2009

Investigation of the role of chromatin dynamics in programming gene expression noise

I am studying genetic determinants of non-genetic variability, or ¬noise,¬î in gene expression using the yeast Saccharomyces cerevisiae.

I started college fully intending to become a physician. However, an excellent first-year interdisciplinary course exposed me to the excitement of research science, and demonstrated the power/utility of using tools from one discipline to study problems in another. I pursued a degree in physics, with the intention of applying the quantitative tools and techniques that I had learned to study biology.

My graduate studies were supervised by both Pam Silver, a molecular and cellular biologist, and Fritz Roth, a statistician and computational biologist. Their joint tutelage allowed me not only to learn fundamental molecular biology and genomics, but also how to analyze data I generated in high-throughput and computational studies. My post-doctoral research on noise in gene expression provides another opportunity to apply mathematical and computational techniques to high-throughput datasets that I am collecting myself. I hope that these studies will provide new insight into problems as fundamental.

Dorethea Kominos Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1992

Expression, purification and x-ray study of src kinase

Magda Maria M. Konarska Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1984

RNA splicing in eukaryotic cell free systems

Erich B. Konrad Jane Coffin Childs Fellow

Stanford University

Appointed in 1971

Enzymatic characterization of E coli mutants

Hyeon-Sook Koo Jane Coffin Childs Fellow

Johns Hopkins University

Appointed in 1988

Effects of DNA bending stress on DNA structure and function

Raphael Kopan Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Appointed in 1990

Mouse Notch

Casey Kopczynski Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1991

Mutations affecting axon outgrowth in the developing nervous system of D melanogaster

Alexei M. Korennykh Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2007

Taking apart a molecular switch: structure, regulation and specificity of the bifunctional kinase-ribonuclease IRE1

Stephen T. Kosak Jane Coffin Childs Fellow

Fred Hutchinson Cancer Center

Appointed in 2002

Nuclear reorganization during erythrocyte development

Michael L. Kotewicz Jane Coffin Childs Fellow

Harvard University

Appointed in 1978

Lambda intergrase

Anna Kotrys, Ph.D. Jane Coffin Childs - HHMI Fellow

Massachusetts General Hospital

Appointed in 2021

Uncovering the molecular mechanisms of mitochondrial heteroplasmy dynamics

Description: Mitochondria are present in nearly all human cells where they play key roles in energy metabolism, biosynthesis, signaling, and cell death. Mitochondrial homeostasis depends on the proper maintenance and expression of the mitochondrial genome (mtDNA). Germline mtDNA mutations can lead to severe, maternally inherited disorders with limited treatment possibilities. Moreover, somatic mtDNA mutations accumulate in neurodegeneration, cancer and aging. mtDNA is a high copy number genome and a mixture of wild-type and mutant mtDNA molecules can co-exist within one cell resulting in “heteroplasmy”. Heteroplasmy dynamics are governed by a complex mix of random drift and selection, but the underlying molecular mechanisms remain unknown. The aim of my post-doctoral research is to uncover the molecular mechanisms that govern mtDNA heteroplasmy. Mechanistic studies of heteroplasmy dynamics will shed the light on the mitochondrial contribution to human health and disease and possibly inspire novel therapeutic approaches to mtDNA disease.

Sharon S. Krag Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1974

Subcellular localization of glycolipid changes during viral transformation

Richard B. Krakaur Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1948

Purification and crystallization of enzymes and proteins

Richard A. Kramer Jane Coffin Childs Fellow

Stanford University

Appointed in 1974

RNA synthesis from fragments of eukaryotic genomes

Edward T. Krementz Jane Coffin Childs Fellow

Yale University

Appointed in 1948

Tumors of neural origin

Thomas M. Kristie Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1987

Repression of enhancer activity by adenovirus E1A

Andrea Kriz, Ph.D. Jane Coffin Childs - HHMI Fellow

Boston Children's Hospital

Appointed in 2022

Dissecting the impact of non-coding somatic mutations in the human brain

While somatic mutations have been heavily studied in tumors, their prevalence and significance to disease risk in healthy individuals is much less well-understood. The Walsh lab and others revealed that somatic mutation is a widespread phenomenon. Human neurons each contain 100 or more clonal somatic single nucleotide variants (sSNV) at birth, acquired during prenatal development, and gain 15-20 additional sSNVs arising per year. Most somatic variants, including those associated with cancer risk, occur in noncoding regions such as enhancers. Despite being the main source of genetic diversity between cells within an individual, the mechanisms by which noncoding somatic mutations form as well as their functional impact are not well understood. My research will focus on developing new strategies to detect rare noncoding somatic variants as well as dissect their epigenomic impact across different cell types in the human brain. This will help illuminate how much this source of variation contributes to cancer risk and brain disease.

Hans Kroeger Jane Coffin Childs Fellow

New York University

Appointed in 1959

Influence of DNA on synthesis of RNA

Claus-Dieter Kuhn Jane Coffin Childs Fellow

Cold Spring Harbor Laboratory

Appointed in 2008

RabGDI displacement factors: mechanism and function in membrane traffic

Urs Kuhnlein Jane Coffin Childs Fellow

Stanford University /
University of Oregon

Appointed in 1970

Enzyme recognition of base sequences on DNA

Richard G. Kulka Jane Coffin Childs Fellow

Case Western Reserve University

Appointed in 1959

Anita Kulukian Jane Coffin Childs Fellow

Stanford University /
Rockefeller University

Appointed in 2010

Centrosomes and the regulation of asymmetric cell division

Dhivya Kumar Jane Coffin Childs Fellow

University of California, San Francisco

Appointed in 2018

Centriolar satellites use phase separation to remodel the centrosome

In animals, the centrosome is the major microtubule organizing center and participates intimately in cell division, organelle positioning and key developmental processes, such as neurogenesis. Consequently, centrosome dysregulation can cause defects in chromosome segregation leading to cancer and defects in brain development leading to microcephaly. Surrounding centrosomes are centriolar satellites, 70-100 nm sized, membrane-less organelles. Their functions are mysterious, although recent evidence from my lab suggests that they participate in the assembly of centrosomes and neurogenesis. The molecular mechanisms by which centriolar satellites participate in centrosome function are unknown. Phase separations have recently been shown to be a biophysical mechanism for partitioning subcellular processes. I hypothesized that centriolar satellites are dynamic, phase-separated compartments and that phase separation is essential for trafficking proteins to remodel the centrosome. To test this hypothesis, I am using biophysical, biochemical, genetic and super-resolution live-cell imaging approaches. My work will reveal how phase separation allows centriolar satellites to act as crucibles in which centrosome-bound proteins are dynamically sorted, providing novel insights into how the centrosome is organized and how this organization goes awry in centrosome-related diseases.

Craig E. Kundrot Jane Coffin Childs Fellow

MRC Center, University Medical School, England /
Yale University

Appointed in 1987

Cloning and crystallization of TFIIIA Zn-binding domains

Patrick C. Kung Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1974

Role of terminal deoxynucleotidyl transferase in developing thymus

Prabhat S. Kunwar Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2008

Genetic dissection of amygdala neuronal circuitry underlying fear and anxiety in mice

My research in the lab of David J. Anderson focuses on genetic dissection of neuronal circuitry underlying defensive and offensive behaviors in mice. We use the latest genetic techniques of neuronal marking, mapping and manipulation in order to explain the neuronal basis of these behaviors.

I was born into a middle-class family in a small town in southern Nepal. After finishing high school in my hometown, I began my undergraduate studies in the biology program of Tri-Chandra College in Kathmandu, Nepal.

I considered scientific research early on, as I realized its power both to explain the natural world and our existence, and to bring practical benefits to society. Soon, I became captivated by the spectacular progress in genetics and biomedical sciences. Not seeing any further academic opportunities in the biomedical sciences in Nepal, I came to the U.S., obtaining my undergraduate degree in biotechnology at the University of Nebraska at Omaha. I then did my PhD under the supervision of Ruth Lehmann at New York University Medical Center. I enjoy traveling, and am also involved in promoting biomedical research and education in Nepal via a biomedical society formed by a group of Nepali scientists.

Lawrence C. Kuo Jane Coffin Childs Fellow

Harvard University

Appointed in 1981

Catalysis and regulation of ornithine transcarbamylase

Scot C. Kuo Jane Coffin Childs Fellow

Washington University in St. Louis /
Duke University Medical Center

Appointed in 1989

Microtubule-dependent motility of organelles

Charlotte Kuperwasser Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 2000

Induction of mammary tumor by p-53-deficient stroma

Kiyoshi Kurahashi Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1955

Formation and metabolism of nucleoside pholyphosphate

Peri Kurshan Jane Coffin Childs Fellow

Stanford University

Appointed in 2011

A search for determinants of synaptic size and function

Stephen E. Kurtz Jane Coffin Childs Fellow

Columbia University

Appointed in 1986

Genetic control of recombination in yeast

Naina Kurup Jane Coffin Childs - HHMI Fellow

Harvard University

Appointed in 2018

Superresolution imaging of age related changes to the neuronal cytoskeleton

With global increases in average lifespan, understanding the neurological changes associated with normal aging has become increasingly relevant. Changes in neuronal architecture and synapse function have been proposed to underlie age related cognitive decline in healthy individuals, although the precise mechanisms remain unclear. The neuronal cytoskeleton is essential to the formation of unique neuronal architectures. Advances in superresolution microscopy have enabled the identification of an evolutionarily conserved Membrane-associated Periodic Skeleton (MPS) that forms an integral part of the neuronal cytoskeleton. Mutations in components of the MPS cause neurodegenerative disorders, suggesting that the presence of this network is also important for the maintenance of neuronal function. My project will focus on dissecting the functional role of age related changes to the MPS, providing us with a better understanding of the progressive loss in cognitive ability widespread in the aging population.

Diana J. Laird Jane Coffin Childs Fellow

Sloan Kettering Institute for Cancer Research

Appointed in 2004

Genetic approaches to primordial germ cell migration

Hubert Lam Jane Coffin Childs Fellow

Brigham and Women's Hospital

Appointed in 2007

Polarity and pathogenesis: identification and characterization of cell polarity determinants in Vibrio cholerae

Keng-Bon Lam Jane Coffin Childs Fellow

Albert Einstein College of Medicine

Appointed in 1973

Yeast mitochondrial nucleic acid metabolism

Teresa M. Lamb Jane Coffin Childs Fellow

Columbia University

Appointed in 1996

Meiotic DNA synthesis and control of meiosis in yeast

Meindert H. Lamers Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2004

DNA pol III holoenzyme structure determination

Terry A. Landers Jane Coffin Childs Fellow

Stanford University

Appointed in 1974

Isolation and characterization of integrated SV40 DNA

Roger S. Lane Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1969

Structure and function of histidine decarboxylase

Matthew Lang Jane Coffin Childs Fellow

Stanford University

Appointed in 1999

Micromechanics of kinesin movement

John P. Langmore Jane Coffin Childs Fellow

MRC Center, University Medical School, England

Appointed in 1975

Localization of chemical sites in biological electron microscopy

Nicholas A. Larsen Jane Coffin Childs Fellow

Harvard University Medical School

Appointed in 2003

Regulation of kinetechore assembly

Benjamin Larson Jane Coffin Childs - Merck Fellow

University of California, San Francisco

Appointed in 2020

Principles of cellular behavior: gait coordination in unicellular walker

I am interested in understanding how cells control shape and movement to thrive in different environments. Although often regarded as simple building blocks, single cells frequently execute surprisingly complex, even animal-like behaviors, which are necessary for proper cellular function. In cells, these behaviors emerge from the joint action of myriad molecular components and interactions between the cell and its environment. How this occurs is poorly understood. To better understand and predict cell behavior, I am working to uncover general principles by studying the coordination of walking in a unicellular organism, the ciliate Euplotes.
How can a single cell, lacking a nervous system, coordinate a gait? While unusual in some ways, Euplotes locomotion is amenable to rigorous behavioral analysis, and many underlying cellular processes and molecular components are deeply conserved among eukaryotes. My work combines theory from computer science and non-equilibrium statistical physics with quantitative microscopy experiments to uncover the mechanisms by which Euplotes coordinates its gait and will develop new theoretical and experimental tools for interrogating the control of complex cellular behaviors.