Shelley Berger is a molecular biologist recognized for research on chromatin biology and epigenetics. Her major research interests are histone and factor post-translational modifications in chromatin regulation and of the tumor suppressor p53; her lab investigates the role of histone modifications in cellular aging and senescence, in cancer, in learning and memory, and underlying organismal level behavior. Berger was born in Detroit, Michigan and graduated from University of Michigan, Ann Arbor, with a B.S. in biology and then with a Ph.D. in Cellular and Molecular Biology. She was a post-doctoral fellow at Harvard University and at Massachusetts Institute of Technology. She joined the faculty at the Wistar Institute in Philadelphia, and there held the Hilary Koprowski Professorship. Berger is currently the Daniel S. Och University Professor at the University of Pennsylvania. She joined the Penn faculty in 2009 as a member of the Departments of Cell & Developmental Biology, Genetics, and Biology. She serves as founding and current director of the Epigenetics Institute in the Penn Perelman School of Medicine. Berger is a fellow of the American Association for Advancement of Science, and is a member the American Academy of Arts and Sciences, the National Academy of Medicine, and the National Academy of Sciences.

Research Interests

Shelley Berger's laboratory is interested in chromatin mechanisms, and principally in histone and transcription factor post-translational modifications, in regulating transcription. Modifications include acetylation, methylation and ubiquitylation, and their combinations and antagonism provide an intricate gene regulatory language. Modifications are translated into emergent properties of normal physiology and disease, including cancer, senescence and aging, and control of memory and complex social behavior. In her laboratory, investigation of epigenetic regulation across this array of questions involves animal models encompassing budding yeast, human cells in culture, mouse, and eusocial ant. Wild type and mutant p53 utilize many chromatin enzymes and epigenetic pathways in normal and cancer cells; such enzymes provide robust, "druggable" targets. During aging there is broad epigenome dysregulation, including disruption of the nuclear lamina with associated chromatin domains, leading to tissue deterioration. Histone acetylation has a crucial role in regulating memory and behavior. Rapid and dynamic histone acetylation in brain neurons is powered by gene-located production of the co-factor acetyl-CoA to fuel acetylation enzymes to induce gene activation - as a potentially unique attribute of differentiated and nondividing cells. The histone acetylation landscape in the normal human aging brain reveals epigenetic protection compared to Alzheimer's disease. Histone acetylation critically alters ant brain function to instruct complex social behavior within the colony.

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Primary Section

Section 41: Medical Genetics, Hematology, and Oncology

Secondary Section

Section 22: Cellular and Developmental Biology