Directory - Jane Coffin Childs Memorial Fund

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Morten Ernebjerg, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Probing complex microbial communities: structure and response to perturbations with antibiotics

Meagan N. Esbin, Ph.D. Jane Coffin Childs Fund

University of Washington

Project Title: Healthy aneuploidy”: Discovering strategies from the placenta to regulate aneuploidy tolerance

Most human cells have two copies of each chromosome, and the loss or gain of entire chromosomes, known as aneuploidy, can often be a characteristic of cancer cells. However, in the placenta, many cells exhibit a high degree of aneuploidy and chromosomal instability. For her fellowship, Dr. Meagan Esbin will study how the cells of the placenta tolerate such high levels of aneuploidy.

During her thesis research, Dr. Esbin studied transcriptional regulation in the joint lab of Drs. Robert Tjian and Xavier Darzacq at UC Berkeley. First, she helped solve the structure of a regulatory hub involved in gene regulation, the human SAGA complex. Then, motivated in part by her passion to improve women’s health and make pregnancy safer, Esbin demonstrated that a human transcription factor (TFEB) plays an essential role in placental cell-cell fusion. This finding reveals new possibilities for rescuing defective cell fusion that can occur in preeclampsia.

In Dr. Min Yang’s lab at the University of Washington, Esbin will take a new angle on understanding placental biology. Using novel cell models, genetic screening, and live imaging she will attempt to define the rules of aneuploidy development and tolerance in the placenta. Her research will provide insight into this life-giving, yet understudied organ. Ultimately, she aims for her research to reveal how we can improve pregnancy outcomes and manage aneuploid cancer cells.

Ellen J. Ezratty, Ph.D. Jane Coffin Childs Fellow

Rockefeller University

Project Title: Stem Cell migration during wound-induced reepithelialization

In my research with Elaine Fuchs, I am studying how the primary cilium regulates the function of epidermal stem cells during embryonic development and wound healing.

I was introduced to nature by my grandmother, who instilled in me a sense of awe for living things as we explored the forests near where I grew up in northwestern Pennsylvania, collecting roots, mushrooms and bugs. ¬†My childhood fascination with nature led me to study biology.

I am interested in how cells interact with and respond to their environment. ¬†¬†In my doctoral research, I tried to understand how the microtubule cytoskeleton controlled the ability of cells to regulate focal adhesions, structures that allow a cell to communicate with its environment during cell migration. For my post-doctoral work, I maintained this interest, but also became fascinated with how stem cells in a tissue are able to ¬ìsense¬î the environmental developmental signals that lead to proper differentiation ¬ó leading me to study the function of the primary cilium in the epidermis. Primary cilia are evolutionarily conserved sensory organelles which act as a cellular antenna, allowing the cell to sample its extracellular environment and process signals that are essential for proper cell growth, development and differentiation.

Dina A. Faddah, Ph.D. Jane Coffin Childs - HHMI Fellow

University of California, San Francisco

Project Title: Genetic identification of a neural circuit that controls salt appetite

Monifa A. Fahie, Ph.D. Jane Coffin Childs Fellow

Brandeis University

Project Title: Translation regulation and viral exploitation in innate immunity

Gordon F. Fairclough, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Alkaline phosphatase structure

Douglas M. Fambrough, Ph.D. Jane Coffin Childs Fellow

Whitehead Institute

Project Title: Parallel analysis of gene expression

Qing R. Fan, Ph.D. Jane Coffin Childs Fellow

Columbia University

Project Title: Structure of follicle stimulating hormone receptor

Rosann A. A. Farber, Ph.D. Jane Coffin Childs Fellow

National Institute for Medical Research

Project Title: Somatic cell genetics and human molecular genetics

Jeffrey A. Farrell, Ph.D. Jane Coffin Childs - Genentech Fellow

Harvard University

Project Title: Novel signaling peptides in zebrafish development

The goal of my project is to identify and characterize novel signals regulating development. Many of the processes taking place during development are controlled by a handful of well-characterized signaling pathways. This observation has led to the belief that most, if not all, of the major developmental signals are known. However, recent genomics projects have identified numerous uncharacterized genes, several of which encode short secreted peptides. A zebrafish mutant generated in one of these peptides, EndE, has a dramatic developmental phenotype, where the embryo forms little or no heart tissue. This suggests that EndE regulates the specification and/or migration of cardiac precursor cells. I will investigate the role of EndE in cardiac development and identify its receptor (Aim 1). Additionally, I will generate mutants for several other novel secreted peptides and analyze their phenotypes (Aim 2). My project will elucidate the role of a novel regulator of heart formation and identify new developmental signaling molecules.

Thomas G. Fazzio, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Lodestar: a metazoan-specific chromatin remodeler

William J. Feaver, Ph.D. Jane Coffin Childs Fellow

University of Texas Southwestern

Project Title: Role of CSA and CSB in transcription/repair coupling

Alexander Fefer, M.D. Jane Coffin Childs Fellow

Karolinska Institutet

Project Title: Investigations concerning cell growth, survival and destruction in a transplantation situation

Renny Feldman, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Nitric oxide signaling in the hypoxic response

Qing Feng, Ph.D. Jane Coffin Childs Fellow

Harvard Medical School

Project Title: Mechanistic dissection of nonsense-mediated decay

Mutations in genes that encode core RNA splicing machinery (such as SF3B1, U2AF1, SRSF2) are frequently associated with hematologic malignancies1–3 (Fig. 1). A number of studies have identified specific splicing defects associated with these mutations4–6, but the impact on gene expression program in these disorders remains poorly understood. Most human transcripts are spliced cotranscriptionally,and revealed previously unknown roles of splicing in regulating transcription7–10. These observations led me to propose that effects of dysregulated splicing on transcription contribute to pathogenesis of cancer. Recently, my new host lab has identified a new regulatory link between splicing and transcription termed “exon-mediated activation of transcription starts” (EMATS)23 (Fiszbein et al.). In brief, they found that inclusion (splicing in) of alternative exons (often found in 5′ UTR) can activate transcription from a proximal upstream alternative promoter (within 1 or 2 kb), showing that expression of such genes is dependent on nearby splicing. However, the precise requirements and mechanistic details are not fully understood. Therefore, I propose to investigate the cis- and trans-acting determinants of EMATS and to use this information to understand the impacts of perturbed splicing on gene expression programs in hematologic malignancies.

Guoping Feng, Ph.D. Jane Coffin Childs Fellow

Washington University School of Medicine

Project Title: Retinotectal synapse formation in transgenic mice

Sheng Feng, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Identification of Small Molecule Ligands for c-Myc mRNA

c-Myc is a transcription factor and an attractive therapeutic target as it drives the majority of human cancers. However, inhibiting c-Myc at the protein level is difficult, in part due to its intrinsically disordered structure. Dr. Sheng Feng aims to circumvent this problem by inhibiting c-Myc mRNA with small molecules. Dr Feng will use a fragment-based approach using an RNA-biased library that is functionalized to improve affinity for RNA. Dr. Feng will tether fragments that bind to adjacent RNA sites to improve binding affinity and selectivity. These experiments will be conducted in Dr. Eric Kool’s lab at Stanford University. Dr. Feng’s research will explore a new route for inhibiting an important target in oncology and represents a general method for inhibiting other difficult protein targets.

As a graduate student in Dr. Stephen Buchwald’s lab at the Massachusetts Institute of Technology, Feng developed copper hydride-catalyzed bond forming reactions that are highly regio- and stereoselective. Such reactions produce important substructures for pharmaceuticals, agrochemicals, and natural products. Dr. Feng’s background in organic chemistry has prepared her to design and prepare small molecule ligand libraries for targeting c-Myc mRNA.

Adam Ray. Fenton, Ph.D. Achelis and Bodman - Jane Coffin Childs Fellow

Weill Cornell Medicine

Project Title: Determining the cause and consequence of cancer cells co-opting neuronal vesicle trafficking mechanisms

Kinesins are motor proteins that “walk” along microtubules to carry cargo inside cells. Adam Fenton, Ph.D., studied how kinesins move mitochondria (the cells’ power source) to where cells need energy. As a Jane Coffin Childs Fellow, he will now investigate a surprising possibility: that a neuron-specific kinesin also helps cancer cells invade other tissues.

In Erika Holzbaur’s and Thomas Jongens’s labs at the University of Pennsylvania, Fenton found several key things about kinesin motors and mitochondrial transport in neurons. In addition to his work on mitochondrial fission in neurons, he learned that a kinesin is turned on by a protein that connects it to mitochondria. He found that some ALS-linked kinesin mutations make this kinesin too active by removing a normal “off” mechanism.

Next, in Samara Reck-Peterson’s lab at Weill Cornell Medicine, Fenton will study cancer progression. Early evidence suggests cancer cells may increase organelle-transport systems that are usually only active in neurons. He will test how a neuron-specific kinesin and its partner proteins contribute to cancer cell invasion and test ways to block this process in tumor organoid models. Fenton anticipates that his research will uncover novel roles for organelle transport in cancer cell biology and may illuminate the path toward new cancer therapies.

Adrian R. Ferre-D'Amare, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Atomic structure of group II self-splicing introns

Diego U. Ferreiro, Ph.D. Jane Coffin Childs Fellow

University of California, San Diego

Project Title: Coupled folding and binding of IkB-alfa

Pamela J. Fink, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: T cell differentiation

David J. Finnegan, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Structure and function of DNA

Harold A. Fisk, Ph.D. Jane Coffin Childs Fellow

University of Colorado, Boulder

Project Title: Characterization of the mouse Mps 1p-like Esk kinase

Elayne M. Fivenson, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Project Title: Illuminating the cell envelope architecture and assembly of a tick-borne pathogen

The bacterial cell surface plays a critical role in bacterial physiology and represents a key target for many antibiotics. However, the properties of many bacterial cell surfaces are not well characterized. Dr. Elayne Fivenson’s fellowship project aims to learn more about the cell surface of Rickettsia parkeri, a tick-transmitted bacteria that is a model system for the more pathogenic species Rickettsia rickettsii that causes the deadly Rocky Mountain Spotted Fever (RMSF).

Fivenson developed her expertise in bacterial cell surfaces in Dr. Thomas Bernhardt’s lab at Harvard Medical School. There, Fivenson demonstrated how an inner membrane protein functions to regulate the synthesis of the outer layer of many Gram-negative bacteria. Next, she investigated how the synthesis of the outer membrane and cell wall are coordinated. While it has long been appreciated that the cell wall impacts cell morphology, Fivenson’s results indicate that the outer membrane also contributes to cell shape.

Now in Dr. Rebecca Lamason’s lab at Massachusetts Institute of Technology, Fivenson will study R. parkeri, a model system for the more pathogenic rickettsial species that cause RMSF. She will use structural and proteomic approaches to reveal the composition of the R. parkeri cell envelope. Then, she will use genetic approaches to dissect cell envelope synthesis pathways with the goal of identifying therapeutic targets. As tick range expands due to climate change, RMSF prevalence has increased. Fivenson’s research promises new insights towards the eventual therapeutic inhibition of these deadly bacteria.

Abraham Flamholz, Jr, Ph.D. Jane Coffin Childs Fellow

California Institute of Technology

Project Title: Developing bacterial bioﬁlms as a model for predicting tissue metabolism

While cells are often studied in suspension or monolayers, more structured forms like tissues and biofilms dominate natural environments. In such settings, the concentrations of critical nutrients like sugars and O2 vary in space and time because cells produce and consume them locally, leading to measurable differences in physiology and gene expression between nearby cells. Spatially structured environments therefore represent many-body systems interacting on multiple timescales through a rich collection of chemical and physical processes. My overriding goal is to determine whether metabolism in mixed biofilms can be predicted quantitatively from simple models with intelligible and measurable parameters. I am currently developing Pseudomonas aeruginosa, a model bacterium that grows in suspension and as a biofilm, as a model for studying metabolic heterogeneity in spatially structured environments. It is commonly assumed that variation in the local O2 concentration is a primary determinant of metabolic heterogeneity in biofilms. As such, I am developing optical approaches to measure local O2 concentrations in real time to test whether a mathematical model can explain O2 dynamics, cell growth, and metabolic rates in biofilms.

Anthony Flamier, Ph.D. Jane Coffin Childs Fellow

Whitehead Institute

Project Title: Formation of phase separated condensates in fragile X-Linked syndromes

Richard B. Flavell, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Mitochondrial biogenesis in Neurospora crassa

Hernan A. Flores-Rozas, Ph.D. Jane Coffin Childs Fellow

Dana-Farber Cancer Institute /
Ludwig Institute for Cancer Research, La Jolla

Project Title: Characterization of a eukaryotic mismatch repair pathway

Linda S. Folley, Ph.D. Jane Coffin Childs Fellow

Cornell University

Project Title: Nuclear control of yeast mitochondrial translation

Jefferson Foote, Ph.D. Jane Coffin Childs Fellow

Medical Research Council (MRC),UKRI

Project Title: Mutational analysis of lysozyme-antilysozyme

Barry M. Forman, M.D., Ph.D. Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Project Title: Retinoid X receptors in oncogenesis

Anthony C. Forster, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Catalytic mechanism of an RNA enzyme

Velia M. Fowler, Ph.D. Jane Coffin Childs Fellow

National Institutes of Health /
The Johns Hopkins University

Project Title: Mechanisms of membrane fusion

Robert O. Fox, Ph.D. Jane Coffin Childs Fellow

University of Oxford /
Yale University

Project Title: NMR analysis of alamethicin conformation in micelles

Barbara S. Fox, Ph.D. Jane Coffin Childs Fellow

National Institute of Health

Project Title: T Cell activation

Donald T. Fox, Ph.D. Jane Coffin Childs Fellow

Carnegie Institution for Science

Project Title: Drosophila hindgut stem cells: uncovering their roles in tissue formation as well as tissue maintenance

Robert T. Fraley, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Liposome-mediated insertion of nucleic acids into cells

Alison R. Frand, Ph.D. Jane Coffin Childs Fellow

Massachusetts General Hospital

Project Title: Genetic control of molting in C. elegans

Mervyn Franklin, Ph.D. Jane Coffin Childs Fellow

Case Western Reserve University

Project Title: Nucleic acids of microorganisms

Jeffrey A. Frelinger, Ph.D. Jane Coffin Childs Fellow

University of Michigan

Project Title: Isolation and characterization of T cell receptors

John G. Frelinger, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Isolation and characterization of T cell receptors

Gerald D. Frenkel, Ph.D. Jane Coffin Childs Fellow

Weizmann Institute of Science, Israel

Project Title: Carcinogenesis

Adam Freund, Ph.D. Jane Coffin Childs Fellow

Stanford University

Project Title: Telomerase trafficking as anti-cancer target

Melvin Fried, Ph.D. Jane Coffin Childs Fellow

Cambridge University

Project Title: Elucidation of mechanisms of enzyme action

Jonathan R. Friedman, Ph.D. Jane Coffin Childs Fellow

University of California, Davis

Project Title: Lateral organization of mitochondrial membranes

Susan J. Friedman, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Drosophila imaginal disc determination

Jonathan M. Friedman, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Crystallization and x-ray analysis

Robert C. Froemke, Ph.D. Jane Coffin Childs Fellow

University of California, San Francisco

Project Title: Disruption of neural circuits by environmental toxins

Susan Froshauer, Ph.D. Jane Coffin Childs Fellow

Yale University

Project Title: Cell biology of Semliki forest virus replication

Michelle Y. Fry, Ph.D. Jane Coffin Childs Fellow

Massachusetts General Hospital

Project Title: In situ cryoET analysis of cristae biogenesis and morphology

Mitochondria generate energy needed to power cells and multicellular organisms. Wrinkles in the inner mitochondrial membrane, known as cristae, concentrate molecular motors for energy production. However, it is unclear how the wrinkly cristae are formed. Dr. Michelle Fry will use a clever approach to investigate cristae formation in cells. She will introduce candidate protein/protein complexes into parasitic protist mitochondria. These mitochondria are smooth, making them amenable for testing with proteins are sufficient to generate cristae. Dr. Fry will use advanced electron microscopy techniques to image changes in mitochondrial morphology. Fry will conduct these studies in Dr. Luke Chao’s lab at Massachusetts General Hospital. These experiments will provide fundamental insights into mitochondrial biology and may provide clues for mitochondrial pathological dysfunction.

As a graduate student in Dr. Bil Clemons lab at the California Institute of Technology, Fry used structural biology to study the targeting of membrane proteins to the endoplasmic reticulum. Specifically, Dr. Fry captured several structural conformations of a protein chaperone, Get3. Fry demonstrated how conformational flexibility is important for Get3 to integrate multiple regulatory signals (binding partners, client proteins, nucleotide binding and hydrolysis). Dr Fry is now excited to use cryo-electron tomography to capture the conformational landscape of proteins that regulate mitochondrial cristae formation in cells.

Yi Fu, Ph.D. HHMI - Jane Coffin Childs Fellow

University of Washington

Project Title: Deciphering the dynamic regulation of mitochondrial genomes

Mitochondria are cellular organelles that house their own DNA. There are hundreds to thousands of copies of the mitochondrial genome (mtDNA) in each cell. Often, mtDNA copies are not the same; rather, a fraction of them carries mutations. Moreover, the composition of mtDNA varies drastically across cells and cell types. Mitochondrial diseases manifest when the pathogenic mutations reach a high percentage in a substantial fraction of cells. However, it is still unclear how mtDNA mutations expand and how cell-to-cell variation of mtDNA composition is formed.

Dr. Yi Fu will address these questions in Dr. Jay Shendure’s lab at the University of Washington. Dr. Fu will develop a method to accurately genotype mtDNA at single-cell resolution and employ this method to monitor mtDNA mutations during differentiation. Fu will also combine this approach with CRISPR perturbation to identify factors that impact the mitochondrial mutation burden in various cell types. These experiments will uncover cell type-specific regulation of mitochondrial genome maintenance. Furthermore, Fu’s research may provide insight into novel therapeutic approaches for mtDNA-associated diseases.

Fu’s expertise in mtDNA stems from her graduate studies in Dr. Agnel Sfeir’s lab at New York University and Memorial Sloan Kettering Cancer Center. There Fu discovered that double-strand breaks in mtDNA activate the integrated stress response, highlighting the cellular program to cope with defective mitochondrial genome. Fu also investigated mtDNA deletions and their impact on cellular metabolism. Now, Fu will leverage genomics and single-cell technologies to elucidate the dynamic regulation of mtDNA during her postdoctoral research.