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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Irene Chiolo, Ph.D.
Department of Biological Sciences
University of Southern California
ABSTRACT
Advancing our knowledge of heterochromatin repair is a high impact investment for improving human health: heterochromatin is a poorly characterized region that comprises nearly a third of the human genome; double-strand break (DSB) repair failures in this region affect not just specific genes but also genome-wide stability; and failures here are a high risk because of the abundance of repeated sequences that characterizes this domain. Our studies in Drosophila cells revealed that ‘safe’ DSB repair by homologous recombination relies on the relocalization of repair sites to the nuclear periphery before strand invasion. The mechanisms responsible for this movement were unknown. Our recent studies revealed that relocalization occurs by directed motion along striking nuclear actin filaments, which are assembled at repair sites by the Arp2/3 complex. Relocalization also requires nuclear myosins associated with the heterochromatin repair complex Smc5/6. This remarkable pathway is conserved in mammalian cells and its defects result in impaired heterochromatin repair, chromosome rearrangements and widespread genome instability. These findings identify de novo nuclear actin filaments and myosins as effectors of chromatin dynamics for heterochromatin repair and stability in multicellular eukaryotes.
