Event date:
Jul 28 2020 9:00 pm

How cell fate decisions are maintained by Polycomb

Dr. Oliver Bell
Transcriptional silencing by Polycomb group (PcG) proteins is a major paradigm for epigenetic inheritance from fly to human. The Polycomb Repressive Complexes PRC1 and PRC2 catalyze distinct chromatin modifications to enforce gene silencing. However, the mechanisms underlying the inheritance of transcriptional silencing by different PRC complexes are not known. Addressing this question has been extremely challenging due to technical limitations that do not discern the initiation from sequence-independent maintenance of repression. We have solved this problem by developing an approach to reversibly recruit PRC1 or PRC2 to transcriptionally inactive or active chromatin in mouse embryonic stem cells. For the first time, we directly and systematically interrogate the ability of different PcG complexes to (1) form repressive chromatin structure, (2) initiate gene silencing, and (3) maintain silencing. I will present an unexpected division of labor between different PRC1 and PRC2 complexes in epigenetic silencing.

Department of Biology initiated a Colloquium series “zooming Molecular and Cellular Biology” where scientists around the world working at the cutting edge are invited as guests. Our inaugural speaker was Dr. Oliver Bell from Keck School of Medicine at the University of Southern California. 

Dr. Oliver Bell is an Assistant Professor in the Dept. of Biochemistry and Molecular Medicine, and the Dept. of Stem Cell and Regenerative Medicine at the Keck School of Medicine at the University of Southern California. His laboratory investigates the epigenetic mechanisms targeting chromatin modification to reinforce maintenance of gene expression states through genome replication. The Bell lab uses synthetic biology approaches, genetics and genomics to manipulate chromatin modifications and study their dynamics and inheritance. Ultimately, Dr. Bell’s research group aims to unravel the crosstalk between epigenetic regulation and cell plasticity.