@article{0c6b60399e4a48fcab52315b0d938943,
title = "Role of yeast SIR genes and mating type in directing DNA double-strand breaks to homologous and non-homologous repair paths",
abstract = "Eukaryotes have acquired many mechanisms to repair DNA double-strand breaks (DSBs) [1]. In the yeast Saccharomyces cerevisiae, this damage can be repaired either by homologous recombination, which depends on the Rad52 protein, or by non-homologous end-joining (NHEJ), which depends on the proteins yKu70 and yKu80 [2,3]. How do cells choose which repair pathway to use? Deletions of the SIR2, SIR3 and SIR4 genes - which are involved in transcriptional silencing at telomeres and HM mating-type loci (HMLα and HMRa) in yeast [4] - have been reported to reduce NHEJ as severely as deletions of genes encoding Ku proteins [5]. Here, we report that the effect of deleting SIR genes is largely attributable to derepression of silent mating-type genes, although Sir proteins do play a minor role in end-joining. When DSBs were made on chromosomes in haploid cells that retain their mating type, sirΔ mutants reduced the frequency of NHEJ by twofold or threefold, although plasmid end-joining was not affected. In diploid cells, sir mutants showed a twofold reduction in the frequency of NHEJ in two assays. Mating type also regulated the efficiency of DSB-induced homologous recombination. In MATa/MATα diploid cells, a DSB induced by HO endonuclease was repaired 98{\%} of the time by gene conversion with the homologous chromosome, whereas in diploid cells with an α mating type (matΔ/MATΔ) repair succeeded only 82{\%} of the time. Mating-type regulation of genes specific to haploid or diploid cells plays a key role in determining which pathways are used to repair DSBs.",
author = "Lee, {Sang Eun} and Fr{\'e}d{\'e}ric P{\^a}ques and Jason Sylvan and Haber, {James E.}",
year = "1999",
month = "7",
day = "15",
doi = "10.1016/S0960-9822(99)80339-X",
language = "English (US)",
volume = "9",
pages = "767--770",
journal = "Current Biology",
issn = "0960-9822",
publisher = "Cell Press",
number = "14",
}