XRS2, a DNA repair gene of Saccharomyces cerevisiae, is needed for meiotic recombination.

Abstract

The XRS2 gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that XRS2 also encodes an essential meiotic function. Spore inviability of xrs2 strains is rescued by a spo13 mutation, but meiotic recombination (both gene conversion and crossing over) is highly depressed in spo13 xrs2 diploids. The xrs2 mutation suppresses spore inviability of a spo13 rad52 strain suggesting that XRS2 acts prior to RAD52 in the meiotic recombination pathway. In agreement with the genetic data, meiosis-specific double-strand breaks at the ARG4 meiotic recombination hotspot are not detected in xrs2 strains. Despite its effects on meiotic recombination, the xrs2 mutation does not prevent mitotic recombination events, including homologous integration of linear DNA, mating-type switching and radiation-induced gene conversion. Moreover, xrs2 strains display a mitotic hyper-rec phenotype. Haploid xrs2 cells fail to carry out G2-repair of gamma-induced lesions, whereas xrs2 diploids are able to perform some diploid-specific repair of these lesions. Meiotic and mitotic phenotypes of xrs2 cells are very similar to those of rad50 cells suggesting that XRS2 is involved in homologous recombination in a way analogous to that of RAD50.

Mutations in XRS2 and RAD50 Delay but Do Not Prevent Mating-Type Switching in Saccharomyces cerevisiae

“…Our results indicate that xrs2 and rad5O cells are proficient in the repair of at least a single chromosomal DSB. This is quite consistent with the observation of a partial diploid-specific repair of corresponding diploid cells to y-irradiation (30,54).…”

“…Previous experiments have shown that meiotic and mitotic phenotypes of xrs2A cells are very similar to those of radSOA cells, implying that XRS2 and RAD5O are involved in homologous recombination in similar ways (30). Here, we confirm these results by showing that xrs2zX affects MAT switching similarly to radSOA, leading us to speculate that XRS2 also encodes or regulates a 5'-to-3' exonuclease activity.…”

“…Alternatively, it is possible that xrs2 and rad5O cells are deficient in the repair of types of radiation-induced DNA damage that are not DSBs. One of the most interesting aspects of radiation response of xrs2 and rad5O cells is that despite the ability of diploid mutant cells to perform some diploid-specific repair, haploid cells are completely deficient in so-called G2 repair, so that the sensitivity of haploid xrs2 and rad5O cells to y-irradiation approaches that of rad52 cells (30). Why haploid and diploid xrs2 and rad5O mutant cells differ in their radiation response remains to be explained.…”

“…Meiotic inviability of xrs2 strains can be rescued by a spol3 mutation, indicating that XRS2 belongs to the group of early meiotic Rec genes, including RAD5O. Accordingly, no meiosis-specific DSBs at the ARG4 hot spot for meiotic gene conversion were detected in xrs2 mutant strains (30). In contrast, mitotic Restriction map of the genomic fragment containing the XRS2 gene on plasmid pEI17 and the construction of deletion-disruption plasmids.…”

“…The XRS2 gene was initially defined by mutations rendering cells sensitive to ionizing radiation and was shown to belong to the RADS2 epistasis group (30,62). In our previous communication (30), we showed that XRS2 was also required for meiotic recombination.…”