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Rad51 Paralogs Remodel Pre-synaptic Rad51 Filaments to Stimulate Homologous Recombination

MR. Taylor, M. Špírek, KR. Chaurasiya, JD. Ward, R. Carzaniga, X. Yu, EH. Egelman, LM. Collinson, D. Rueda, L. Krejci, SJ. Boulton,

. 2015 ; 162 (2) : 271-86.

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc16000083
E-zdroje Online Plný text

NLK Cell Press Free Archives od 1995-01-01 do Před 1 rokem
Free Medical Journals od 1995 do Před 1 rokem
Open Access Digital Library od 1995-01-01
Elsevier Open Access Journals od 1995-01-13 do 2023-06-22
Elsevier Open Archive Journals od 1995-01-13 do Před 1 rokem

Odkazy

PubMed 26186187
DOI 10.1016/j.cell.2015.06.015
Knihovny.cz E-zdroje

Repair of DNA double strand breaks by homologous recombination (HR) is initiated by Rad51 filament nucleation on single-stranded DNA (ssDNA), which catalyzes strand exchange with homologous duplex DNA. BRCA2 and the Rad51 paralogs are tumor suppressors and critical mediators of Rad51. To gain insight into Rad51 paralog function, we investigated a heterodimeric Rad51 paralog complex, RFS-1/RIP-1, and uncovered the molecular basis by which Rad51 paralogs promote HR. Unlike BRCA2, which nucleates RAD-51-ssDNA filaments, RFS-1/RIP-1 binds and remodels pre-synaptic filaments to a stabilized, "open," and flexible conformation, in which the ssDNA is more accessible to nuclease digestion and RAD-51 dissociation rate is reduced. Walker box mutations in RFS-1, which abolish filament remodeling, fail to stimulate RAD-51 strand exchange activity, demonstrating that remodeling is essential for RFS-1/RIP-1 function. We propose that Rad51 paralogs stimulate HR by remodeling the Rad51 filament, priming it for strand exchange with the template duplex.

Citace poskytuje Crossref.org

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