@article{Taylor:2015:10.1016/j.cell.2015.06.015,
author = {Taylor, MRG and Spirek, M and Chaurasiya, KR and Ward, JD and Carzaniga, R and Yu, X and Egelman, EH and Collinson, LM and Rueda, D and Krejci, L and Boulton, SJ},
doi = {10.1016/j.cell.2015.06.015},
journal = {Cell},
pages = {271--286},
title = {Rad51 Paralogs Remodel Pre-synaptic Rad51 Filaments to Stimulate Homologous Recombination},
url = {http://dx.doi.org/10.1016/j.cell.2015.06.015},
volume = {162},
year = {2015}
}

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TY  - JOUR
AB  - 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.
AU  - Taylor,MRG
AU  - Spirek,M
AU  - Chaurasiya,KR
AU  - Ward,JD
AU  - Carzaniga,R
AU  - Yu,X
AU  - Egelman,EH
AU  - Collinson,LM
AU  - Rueda,D
AU  - Krejci,L
AU  - Boulton,SJ
DO  - 10.1016/j.cell.2015.06.015
EP  - 286
PY  - 2015///
SN  - 0092-8674
SP  - 271
TI  - Rad51 Paralogs Remodel Pre-synaptic Rad51 Filaments to Stimulate Homologous Recombination
T2  - Cell
UR  - http://dx.doi.org/10.1016/j.cell.2015.06.015
VL  - 162
ER  - 

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