2024-03-29T00:59:29Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1658442018-06-08T00:56:47Zcom_10261_134com_10261_1col_10261_513
00925njm 22002777a 4500
dc
Cabello-Lobato, María J.
author
Cano-Linares, María I.
author
González-Prieto, Román
author
Prado, Félix
author
2016
The recombination proteins Rad52 and Rad51 help the fork to pass through blocking lesions and to fill in the gaps of ssDNA generated during the process of lesion bypass. Their recruitment to the ssDNA lesions has obligatorily to occur during S phase. Here we show that Rad52 and Rad51 display the same kinetics of chromatin binding as the helicase Mcm2-7: they accumulate in G1, are released during replication, and remain bound to chromatin in the presence of replicative blocking lesions. This coordinated response requires Cdc7-dependent physical interactions between Rad51/Rad52 and the Mcm2-7 helicases that are not at the fork. Accordingly, reducing Cdc7 activity impairs sister-chromatid junction formation and ssDNA filling by recombination. Therefore, the loading of Rad51 and Rad52 in G1, together with a Mcm2-7-mediated mechanism that couples the fork advance with Rad52/Rad51 binding to replicative damage, provides a strategy to ensure the filling of the ssDNA lesions through an error-free repair mechanism.
XXXIX Congreso SEBBM (2016)
http://hdl.handle.net/10261/165844
A mechanism for the recruitment of recombination proteins during DNA damage tolerance