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Rad51 and Rad52 supply to replicative DNA lesions relies on cell cycle regulated interactions with the Mcm2-7 helicase

AutorCabello-Lobato, María J. ; Cano-Linares, María I.; González-Prieto, Román ; Prado, Félix
Fecha de publicación2017
CitaciónEMBO Conference: The DNA damage response in cell physiology and disease (2017)
ResumenThe recombination proteins Rad51 and Rad52 help the fork to bypass blocking lesions and fill in the gaps of ssDNA generated during this process of DNA damage tolerance (DDT). Their recruitment to the ssDNA lesions must occur during S phase. Here we show that Rad51, Rad52 and the Mcm2-7 helicase display similar patterns of chromatin binding: they accumulate in G1, are released during replication and remain bound to chromatin in the presence of replicative blocking lesions. Moreover, their binding to chromatin during S phase requires the kinase activity of Cdc7. This kinetics of chromatin binding is coordinated through physical interactions between Rad51 and Rad52 with Mcm2-7. These interactions are prevented at the pre-replication complex and at the replication fork, suggesting that they occur with the excess of Mcm2-7 helicases that are loaded in G1. Importantly, Cdc7-mediated Mcm2-7/Rad51/Rad52 accumulation at chromatin is required for ssDNA filling by recombination, supporting the relevance of these interactions and providing new functions for Cdc7 in DDT. We propose that chromatin recruitment of Rad51/Rad52 in G1, together with a mechanism mediated by Mcm2-7 to supply Rad51/Rad52 to replicative ssDNA lesions, provide a strategy for ensuring that ssDNA lesions are filled via an error-free repair mechanism.
DescripciónResumen del póster presentado a la EMBO Conference: The DNA damage response in cell physiology and disease, celebrada en Atenas (Grecia) del 2 al 6 de octubre de 2017.
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