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Epigenetics, chromosome dynamics, and disease

Eukaryotic genomes are condensed into chromatin fibers in order to fit over a meter of DNA within the limited volume of the nucleus.  However, chromatin assembly limits the accessibility of genomic sequences and creates inherent barriers for nuclear events such as transcription, DNA replication, and DNA repair.  Consequently, chromatin structure must be dynamic or fluid, and local changes in chromatin structure are regulated to to provide the cell with profoundly effective methods for fine-tuning DNA metabolism. Different chromatin states can be inherited by progeny after cell division, providing epigenetic regulation of both coding and noncoding RNAs that control cell function and identity. Not too surprisingly, disruption of mechanisms that control chromatin dynamics can lead to aberrant gene expression, improper or nonexistent DNA repair, chromosomal translocations, inappropriate proliferation, developmental errors, onocogenesis, or even cell death. Scientists in the Program in Molecular Medicine are investigating these mechanisms in detail, uncovering new insights that are enabling the development of therapeutic strategies for attacking cancer and other major diseases.

Bach Lab
Our research investigates molecular and epigenetic mechanisms of gene expression during cell fate specification. We use mouse embryogenesis as model system applying molecular, biochemical and genetic methods. (Bach profile)

Benanti Lab
Our laboratory is interested in the molecular mechanisms that control how cells grow and divide. We are using genetics, biochemistry and cell biology, in both yeast and mammalian cells, to study how protein degradation by the ubiquitin proteasome system controls cell cycle and metabolic transitions.  (Benanti profile)

Brodsky Lab
We use Drosophila melanogaster as a model organism to study how cells distinguish between normal and dysfunctional chromosomes. We are particularly interested in how p53-dependent and p53-independent signaling pathways regulate apoptosis in response to DNA damage and unprotected telomeres.  (Brodsky profile)

Doxsey Lab
Our laboratory investigates the mechanisms of centrosome function, spindle organization, cell cycle  progression/checkpoints, cell separation during cytokinesis and asymmetries generated during mitosis. We are interested in the relationship of these processes to cancer, stem cell self-renewal, cancer stem cells and human aging. (Doxsey profile)

Fazzio Lab
Our lab is focused on the identification of regulatory networks controlling gene expression in stem cells. In particular, we are interested in the roles of chromatin regulators in stem cell self-renewal and differentiation, and we take molecular, genomic, and biochemical approaches to understand these processes. (Fazzio profile)

Garber Lab
Manuel Garber, PhD, associate professor of molecular medicine and bioinformatics and integrative biology, and director of the Bioinformatics Core. Dr. Garber’s methods have been critical to the discovery and characterization of a novel set of large intergenic non-coding RNAs (lincRNAs) and to our understanding of the immune transcriptional response to pathogens. In September 2012, Dr. Garber moved to the University of Massachusetts Medical School to establish his laboratory and direct the Bioinformatics core.  (Garber profile)

Kaufman Lab
We study several different classes of proteins used by eukaryotic cells to deposit histones onto DNA, as well as enzyme complexes that chemically modify chromosome proteins in order to alter DNA accessibility. We study these processes in yeast and human cells, using biochemical, genetic, genomic, and cell biological techniques.  (Kaufman profile)

Luban Lab
Distinguished physician–scientist Jeremy Luban, MD has been appointed professor of molecular medicine at UMass Chan Medical School and the David L. Freelander Memorial Professor in HIV/AIDS Research. Dr. Luban’s  research focuses on understanding host cell factors that contribute to HIV viral replication. He has identified Cyclophilin A and Trim 5 among more than thirty HIV-1 regulatory host factors. His work will contribute to the development of drugs and vaccines targeting HIV virus infections and other disease states. NIH/NIDA named him a 2012 Avant-Garde Awardee for HIV/AIDS research.  (Luban profile)

Maehr Lab
Type 1 Diabetes (T1D) is the result of an autoimmune destruction of insulin producing, pancreatic beta cells. The events leading to the disease have usually occurred long before diagnosis and are based on complex interactions between genes and the environment. The currently available rodent models for T1D can only represent a limited number of patients leaving open the question how many different types of T1D exist. To overcome these difficulties and expand our understanding of T1D and other diseases targeting the immune system we are building in vitro models using human pluripotent stem cells. In those stem cell-based model systems genetic and developmental aspects of the disease can be elucidated. The long-term goal is to recapitulate the disease in a patient-specific manner and to identify novel treatment strategies. (Maehr profile)

Peterson Lab
Work in the lab is focused on understanding how chromosome structure influences gene transcription, DNA replication and repair, with special emphasis on identifying and characterizing the cellular machines that control chromosome dynamics. We use a combination of chromatin biochemistry, analytical ultracentrifugation, and yeast molecular genetics. (Peterson profile)

Theurkauf Lab
Work in the lab addresses RNA localization and embryonic patterning, the response of mitotic cells to DNA damage, and small RNA function in germline development. Studies combine high resolution imaging, genetic, and molecular approaches in Drosophila and mammalian cultured cell systems.  (Theurkauf profile)

Walker Lab
Using C. elegans and mammalian models, we study how lipid homeostasis is affected by genetics or diet and how transcriptional control of methyl donor supply may affect cellular processes such as epigenetics. We also examine links between metabolism and cellular function potentially contributing to human metabolic disorders.  (Walker profile)