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SGSl, a Homologue of the Bloom’s and Werner’s Syndrome Genes, Is Required for Maintenance of Genome Stability in Saccharomyces cereuiSiae

The Saccharomyces cerevisiae SGSl gene is homologous to Escherichia coli RecQ and the human BLM and WRN proteins that are defective in the cancer-prone disorder Bloom’s syndrome and the premature aging disorder Werner’s syndrome, respectively. While recQmutants are deficient in conjugational recombination and DNA repair, Bloom’s syndrome cell lines show hyperrecombination. Bloom’s and Werner’s syndrome cell lines both exhibit chromosomal instability. sgslA strains show mitotic hyperrecombination, as do Bloom’s cells. This was manifested as an increase in the frequency of interchromosomal homologous recombination, intrachromosomal excision recombination, and ectopic recombination. Hyperrecombination was partially independent of both RAD52 and RADI. Meiotic recombination was not increased in sgslA mutants, although meiosis I chromosome missegregation has been shown to be elevated. sgslA suppresses the slow growth of a t q 3 A strain lacking topoisomerase 111. Although there was an increase in subtelomeric Y’ instability in sgslA strains due to hyperrecombination, no evidence was found for an increase in the instability of terminal telomeric sequences in a top3A or a sgslA strain. This contrasts with the telomere maintenance defects of Werner’s patients. We conclude that the SGSI gene product is involved in the maintenance of genome stability in S. cermisiae.