| Literature DB >> 20122407 |
Jordan D Ward1, Diego M Muzzini, Mark I R Petalcorin, Enrique Martinez-Perez, Julie S Martin, Paolo Plevani, Giuseppe Cassata, Federica Marini, Simon J Boulton.
Abstract
Homologous recombination (HR) is essential for repair of meiotic DNA double-strand breaks (DSBs). Although the mechanisms of RAD-51-DNA filament assembly and strand exchange are well characterized, the subsequent steps of HR are less well defined. Here, we describe a synthetic lethal interaction between the C. elegans helicase helq-1 and RAD-51 paralog rfs-1, which results in a block to meiotic DSB repair after strand invasion. Whereas RAD-51-ssDNA filaments assemble at meiotic DSBs with normal kinetics in helq-1, rfs-1 double mutants, persistence of RAD-51 foci and genetic interactions with rtel-1 suggest a failure to disassemble RAD-51 from strand invasion intermediates. Indeed, purified HELQ-1 and RFS-1 independently bind to and promote the disassembly of RAD-51 from double-stranded, but not single-stranded, DNA filaments via distinct mechanisms in vitro. These results indicate that two compensating activities are required to promote postsynaptic RAD-51 filament disassembly, which are collectively essential for completion of meiotic DSB repair. Copyright 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID: 20122407 DOI: 10.1016/j.molcel.2009.12.026
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970