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Subramanian Lab
Diverse cellular functions such as mitosis, cell migration, and differentiation rely on the dynamic assembly of the microtubule cytoskeleton into distinct architectures.  We combine high-resolution fluorescence-microscopy based assays with quantitative biochemical and structural methods to dissect the molecular mechanisms underlying the organization of functional micron-length scale cytoskeletal structures from the collective activity of nanometer-sized proteins.
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Alt Lab
The Alt laboratory studies mechanisms that maintain genomic stability in mammalian cells. The programmed recombination and hypermutation events in lymphocytes and the general DNA repair mechanisms involved in these processes are a focus. The laboratory also studies mechanisms that promote and prevent oncogenic translocations.  Approaches range from molecular genetics and biochemistry to animal models.
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The Altshuler lab studies human genetic variation and develops laboratory and analytical methods for associating genotype and phenotype. Our main focus is type 2 diabetes, with projects in prostate cancer, lupus, and other diseases. Long-term, we hope to apply genetic information to improve diagnostics and therapeutics in the clinic.
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The Ausubel laboratory uses genetic, genomic, and chemical genetic approaches to: (1) elucidate the molecular basis of microbial pathogenesis in the bacterial pathogens Pseudomonas aeruginosa and Pseudomonas syringae and (2) identify the components of the signaling pathways involved in the host innate immune response in the plant Arabidopsis thaliana and the nematode Caenorhabditis elegans.
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In erythrocytes, Protein 4.1R is essential for membrane integrity. Deficiencies cause congenital hemolytic anemia. We have shown that there are many isoforms of P4.1R in other tissues. These participate in the mitotic apparatus, costameres, tight junctions, and adherens junctions. We are studying the structure function relationships of these isoforms. We also study the regulated pre-mRNA splicing events that govern their tissue and differentiation stage expression.
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We use the nematode C. elegans to study processes that defend against environmental, metabolic, and proteotoxic stress, and how these stress defenses influence aging. We are particularly interested in understanding mechanisms that regulate these stress defenses at the level of gene expression, and in how growth and nutrient signals influence these regulatory mechanisms
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The Blower Lab is interested in understanding both how and why RNA is targeted to microtubules during mitosis. We primarily use cell free extracts from the African clawed frog Xenopus laevis to study how RNA influences the assembly of microtubules into a dynamic bipolar spindle.
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Constance Cepko and her colleagues study the development of the central nervous system of vertebrates, with an emphasis on the development of the retina. They are also studying the mechanisms of photoreceptor degeneration, and working towards gene therapy for prevention of blindness.
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We use quantitative whole genome and proteome measures to guide computational modeling of regulatory and enzymatic networks in microbial and mammalian cells. We develop technologies based on bioinformatics, microarrays, mass-spectrometry, automation, multiplexing, microfluidics, and homologous-recombination genome engineering. We have recently used these to discover new regulatory motifs involved in cell-cycle control, stress response, and many other network components.
We are interested in understanding the molecular mechanisms that control and coordinate transcription and co-transcriptional processes, including splicing, chromatin remodeling and termination. We develop genomic approaches to study these questions, such as nascent elongating transcript sequencing (NET-seq), which provides a quantitative measure of RNA polymerase density across the genome with single nucleotide precision.
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We are investigating mechanisms underlying germline maintenance and accurate meiotic chromosome segregation at the molecular level. We are exploring meiotic chromosome dynamics, particularly, the interplay between changes in chromosome configuration/structure during meiosis, and homologous chromosome pairing, synapsis, and DNA double-strand break repair. We are also investigating the roles of histone demethylases in germline maintenance and double-strand break repair. Our studies combine genetic,...
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Research in the Dymecki laboratory explores the development and function of brainstem neural systems including: the serotonergic system, with its involvement in behaviors ranging from respiratory control to aggression; the precerebellar system, with its central role in coordinating locomotor behavior; and the hindbrain choroid plexus, as an organizing center during hindbrain development and as a source of cerebral spinal fluid. We study these areas in mice using a range of novel genetic, embryological and...
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We study the cellular response to genotoxic stress. We have uncovered a signal transduction protein kinase cascade that phosphorylates over 700 proteins in response to DNA damage and controls genomic stability. Using synthetic biology we also develop genetic technologies such as genome-wide viral libraries of shRNAs for genetic screening in mammals to identify genes important for cancer and growth control.
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 We study TNF-induced fate decisions in mammalian cells. TNF is particularly interesting because it induces both pro-survival and prodeath signals. Combining mathematical modeling and single-cell measurements, we exploit variability in response in a cell population to explore how these signals are integrated in time and space to control cell fate.
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Our focus is on "random" monoallelic expression, an autosomal analog of X inactivation.  Mechanisms of this type control genes coding for cytokines, immunoglobulins and olfactory receptors, and are crucial for the generation of cell diversity in the immune and nervous systems.  We have shown that this type of allelic choice occurs with many hundreds of human genes, creating an unexpected epigenetic diversity in cell populations.
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Animal genomes endow cells and circuits with the ability to form life-long memories.  How does a genome orchestrate this dynamic interaction of neurons with experience?  The genome responds to experience by unleashing bursts of new gene expression that rewire circuits to store long-term memories.  We are applying genetic, genomic, electrophysiological, and behavioral tools to understand this process.
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Dr. James F. Gusella, born and raised in Ottawa, Canada, received a B.Sc. in Honours Biology from the University of Ottawa in 1974. He continued his education at the University of Toronto, where he earned a M.Sc. degree in Medical Biophysics in 1976 and at the Massachusetts Institute of Technology, where he received his Ph.D. in Biology in 1980.
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The Harris laboratory is interested in the control of growth and proportion in the development of the skeleton.   The lab uses the zebrafish as a model system to probe the genetic basis of this control.  
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Heiman Lab
We are interested in the basis of cellular architecture – that is, how a cell gets its shape. For example, how does a neuron know how long its dendrites need to be to reach their targets? How do cells of diverse types coordinate their shapes in order to assemble an organ? We take advantage of the highly stereotyped development of the nematode C. elegans to identify the genetic programs that specify the shape of a cell and the contacts it makes with its neighbors.
Joel Hirschhorn, Ph.D.
We aim to understand the genetic basis of traits related to body size (obesity, height and pubertal timing), and certain common diseases (diabetic nephropathy and asthma).  We use association studies, informed by population genetics, statistical considerations and gene expression data, to identify genes that influence these polygenic traits in humans.
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Kennedy Lab
Epigenetic processes regulate many facets of biology and underlie the etiology of many human diseases. Small non-coding RNAs are important regulators of gene expression in eukaryotes. We have shown that small RNAs act as informational vectors to direct the inheritance of epigenetic information across generations.
Carla Bender Kim, Ph.D.
The broad interest of our lab is to characterize the biology of stem cells in normal lung and lung cancer. We use a combination of mouse genetics, cell biology and genomics approaches in our studies. We hypothesize that lung stem cell biology will contribute to understanding the cellular and molecular basis of lung diseases.
Robert E. Kingston, Ph.D.
The Kingston lab is interested in understanding the fundamental mechanisms of how eukaryotic enzymes can modify chromatin. One focused approach is to isolate chromatin-modifying proteins and to test such complexes in functional assays, with the thesis that assay outcomes will inform the in vivo function of these protien machines. Another important goal is to understand how long-range chromatin interactions are established in the cell nucleus, and this effort is leading to new strategies towards defining...
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The Kucherlapati laboratory is involved in cloning and characterization of human disease genes with a focus on human syndromes with a significant cardiovascular involvement, use of genetic/genomic approaches to understand the biology of cancer and the generation and characterization of genetically modified mouse models for cancer and other human disorders.
Louis M. Kunkel, Ph.D.
The Kunkel laboratory works on understanding the pathogenesis and genetics underlying the muscular dystrophies. They are attempting therapy of the muscular dystrophies in mice through the use of adult stem cells from muscle. Recently, they have developed zebrafish models of the human dystrophies in an attempt to screen for suppressor mutations. They have also expanded their genetic research into looking at complex disease traits such as Autism and Interstitial Cystitis.
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We study chromatin organization and epigenetic regulation, using X chromosome dosage compensation in Drosophila as a model system. Studies of dosage compensation in mammals and fruitflies suggest that RNAs can play a key role in chromosomal targeting of chromatin modifying complexes. The mechanistic roles of the RNAs within such complexes remain to be understood.
Jeannie T. Lee, M.D., Ph.D.
Our lab studies how male (XY) and female (XX) cells use a mechanism called X-chromosome inactivation to achieve equality of sex chromosome gene expression. Our studies are focused on three noncoding RNA loci whose actions coordinate the many steps of X-chromosome inactivation. We are also interested in the mechanistic and evolutionary relationship between X inactivation and imprinting. Recent work by the Lee Lab suggests that imprinted X-chromosome inactivation is directly connected to meiotic sex...
David M. Livingston, M.D.
Livingston Lab
My laboratory works on the elucidation of pathways that are controlled by a growing family of breast and ovarian cancer suppressor genes. This family, which includes BRCA1 and 2,  encode proteins that, at a minimum, contribute to the normal cellular responses to DNA damage and to genome integrity control, in general. In particular, we have emphasized an effort to understand how the functions of these gene products contribute to breast and ovarian cancer suppression, in particular.
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We study how the human genome varies in structure and how such structural and copy-number variation influences molecular phenotypes in cells and disease risk in populations. We develop experimental technology for discovering and typing genome structural variants. We recently discovered large, common deletion polymorphisms that appear to influence body weight and Crohn's disease via regulatory effects on nearby genes, and are working to understand how these and other regulatory polymorphisms influence human...
Marjorie Oettinger, Ph.D.
The various projects in my laboratory are connected by one central theme: we seek to understand all facets of the V(D)J rearrangements that generate diversity within the vertebrate immune system. Specifically we are studying the enzymatic and regulatory machinery involved, the mechanism of the reaction, and the role of chromatin structure in the regulation of recombination events during lymphoid development. In addition, we are interested in how errors in this process lead to various human diseases.
Norbert Perrimon, Ph.D.
The general interest of our laboratory is to understand the mechanisms by which cells and tissues talk to each other to coordinate the formation of specific structures during development and to maintain homeostasis. We study these questions in Drosophila using classic genetics as well as state-of-the-art genomic and proteomic methodologies. Current interests are in muscle development, cell migration and stem cell biology.
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The Reich laboratory studies population mixture as a foundation for medical, evolutionary and population genetics. Human population history is often explained as a series of “splits”: the divergence of human and chimpanzee ancestors 5-7 million years ago, the spread of modern humans into Eurasia 40,000-100,000 years ago, and the spread into the Americas by at least 15,000 years ago.
Gary Ruvkun, Ph.D.
 The Ruvkun lab uses C. elegans molecular genetics and genomics to study miRNA and RNAi pathways. We also use genome-wide RNAi analysis to study various biological process in C. elegans including molting, insulin signaling, fat deposition, and longevity. Finally we are developing protocols and instruments that use PCR primers corresponding to universal sequence elements to search for diverse microbes from extreme environments.
Brian Seed, Ph.D.
Seed Lab
Our lab is using new technologies to couple rapid identification of interesting genes with methods for studying the consequences of their expression in an organismic context. We have developed an efficient type of expression cloning of signal transduction intermediates that allows us to rapidly identify cDNAs encoding genes that engage a number of known transduction pathways. In addition, we continue to work on methods for creating mutant cell lines that have lesions in signal transduction pathways, and on...
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Christine Seidman is interested in dominant-acting mutations in sarcomere protein genes that cause hypertrophic cardiomyopathy in humans. The Seidman lab has made a murine model of this disease and demonstrated that these mutations lead to altered Ca2+ concentrations in myocytes. Ca2+ channel blockers reduce the hypertrophic response to sarcomere protein gene mutations in mice.
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Jonathan Seidman is interested in dominant-acting mutations in sarcomere protein genes that cause hypertrophic cardiomyopathy in humans. The Seidman lab has made a murine model of this disease and demonstrated that these mutations lead to altered Ca2+ concentrations in myocytes. Ca2+ channel blockers reduce the hypertrophic response to sarcomere protein gene mutations in mice.
Jen Sheen, Ph.D.
 Our laboratory is interested in the molecular mechanisms underlying plant responses to growth and stress hormones, nutrients, environmental stresses, and pathogens. We use a combination of genetic, genomic, biochemical and cellular approaches to discover key regulatory genes, and elucidate their functions and actions in the control of these central signal transduction pathways from receptors/sensors to transcription factors and target genes in plants.
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Our laboratory studies the role of the core cell cycle machinery in mouse development and in cancer using genetic, genomic, and proteomic approaches. The overall goal is to understand how cell proliferation is controlled, how cancer cell cycles differ from normal ones, and how we can explore these differences for cancer therapy. We also study non-cell cycle functions played by the cell cycle machinery.
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The Sinclair laboratory studies molecular mechanisms and small molecules that slow the pace of aging and age-related diseases. We focus on longevity genes and pharmacological approaches that increase the body's natural defenses against diseases such as cancer, Alzheimer's, infertility, type II diabetes and obesity. We study the contribution of these pathways to the health benefits of a low calorie diet and of exercise. Approaches include biophysics, biochemistry, cell culture, and mouse...
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My laboratory research is focused on the origin, early evolution and laboratory synthesis of life, and the in vitro directed evolution of functional biopolymers.
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The laboratory studies the genetic basis by which form and structure are regulated during vertebrate development. We combine classical methods of experimental embryology with modern molecular and genetic techniques for regulating gene expression during embryogenesis.
Marc Vidal, Ph.D.
Our goals are to understand how protein interaction, or “interactome”, networks are organized at the scale of the whole cell, how such global organization contributes to biological processes, how the interactome varies in time and space, and how perturbations in interactome networks contribute to human disease.
Matthew L. Warman, M.D.
Warman Lab
Members of the Warman laboratory are committed to identifying genetic causes of skeletal disease, to understanding how the responsible genes participate in the biologic processes of skeletal growth and homeostasis, and to using this knowledge to improve human health. Patients affected by genetic disorders of the skeleton are the impetus for scientific inquiry in the Warman lab, but in addition to the human genetic approach, the lab also relies on model organism approaches, and cellular, biochemical,...
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Research in our laboratory focuses on understanding eukaryotic gene expression and chromatin structure, using the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe.
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We study the mechanisms by which homologous chromosomal regions/genes/sequences influence each other at the level of chromosome behavior, genome integrity, gene expression, and chromatin structure. To this end, we conduct genetic, molecular, and bioinformatic analyses, focusing on homologue pairing, transvection (such as enhancer action in trans), mitotic recombination, ultraconserved elements, dosage, and chromatin structure in Drosophila and humans.
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The overall goal of our research is to achieve a greater understanding of the molecular basis of brain aging and how normal aging transitions to pathological aging, giving rise to neurodegenerative disorders such as Alzheimer's and Parkinson's disease. This frequently involves interdisciplinary approaches with collaborations between molecular and computational biologists, both within the lab and with other labs. The approaches range from molecular and cell biological studies in vitro to the analysis of...
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Our lab is interested in (1) how epigenetic modification-mediated dynamic changes in chromatin structure affect gene expression, cell lineage commitment, stem cell pluripotency/self-renewal, (2) epigenetic mechanism of drug addiction, and (3) how misregulation of epigenetic factors contributes to the development of diseases such as diabetes, neurological diseases, and cancer. Our long-term goal is to apply what we learn in basic research to treatments of human diseases.