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Covalent modifications to DNA and the histone packaging proteins allow chromatin to act as a dynamic signaling platform to regulate genomic DNA access and ultimately establish and maintain cellular phenotypes. Moreover, there is increasing appreciation that chromatin alterations per se, including DNA and histone modifications, are involved in the pathogenesis of cancer. Nowhere is this better supported than with the groundbreaking discoveries of high-frequency, somatic mutations in histones that are drivers of oncogenesis. These mutations (collectively called ‘oncohistones’) cause amino acid substitutions that localize to conserved residues in the N-terminal tail of histone H3 and all seem to be linked, either directly or indirectly, to disruption of normal levels and distribution of histone H3 methylation and thus genomic regulation. We are currently using a combination of biochemical, epigenomic and transcriptomic approaches, along with defined cell lines to understand how histone H3 lead to altered chromatin states that profoundly influence gene expression patterns. I will discuss some of our recent work on how histone mutations perturb cellular differentiation through inhibition of specific chromatin-modifying enzymes.
Peter W. Lewis, Ph.D., received a doctorate in molecular and cell biology in 2006 from the University of California, Berkeley, where he worked with Dr. Michael Botchan. From 2007 to 2013, he conducted postdoctoral studies at Rockefeller University in the laboratory of Dr. C. David Allis. He then accepted a position as an assistant professor of biomolecular chemistry at the University of Wisconsin in Madison.
Peter Lewis, Ph.D.
Assistant Professor, Department of Biomolecular Chemistry
School of Medicine and Public Health
University of Wisconsin-Madison
12:00 pm at Van Andel Institute
Conference Room 3104/3105
For questions, please contact Kim Cousineau at 616.234.5684.