Nucleic Acids Research Advance Access published online on September 28, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm488
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Molecular Biology |
Different genetic requirements for repair of replication-born double-strand breaks by sister-chromatid recombination and break-induced replication
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, and Departamento de Biología Molecular, CABIMER, CSIC-Universidad de Sevilla, Av. Américo Vespucio s/n, 41092 SEVILLA, Spain
*To whom correspondence should be addressed. Tel: +34 954 468 372; Fax: +34 954 461 664; Email: aguilo{at}us.es
Received April 28, 2007. Revised June 4, 2007. Accepted June 5, 2007.
Homologous recombination (HR) is the major mechanism used to repair double-strand breaks (DSBs) that result from replication, but a study of repair of DSBs specifically induced during S-phase is lacking. Using an inverted-repeat assay in which a DSB is generated by the encountering of the replication fork with nicks, we can physically detect repair by sister-chromatid recombination (SCR) and intra-chromatid break-induced replication (IC-BIR). As expected, both events depend on Rad52, but, in contrast to previous data, both require Rad59, suggesting a prominent role of Rad59 in repair of replication-born DSBs. In the absence of Rad51, SCR is severely affected while IC-BIR increases, a phenotype that is also observed in the absence of Rad54 but not of its paralog Rdh54/Tid1. These data are consistent with SCR occurring by Rad51-dependent mechanisms assisted by Rad54, and indicate that in the absence of strand exchange-dependent SCR, breaks can be channeled to IC-BIR, which works efficiently in the absence of Rad51. Our study provides molecular evidence for inversions between repeats occurring by BIR followed by single-strand annealing (SSA) in the absence of strand exchange.
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