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Abstract
The SGS1 gene of Saccharomyces cerevisiaeis a homologue for the Bloom's syndrome and Werner's syndrome genes. The disruption of the SGS1 gene resulted in very poor sporulation, and the majority of the cells were arrested at the mononucleated stage. The recombination frequency measured by a return-to-growth assay was reduced considerably in sgs1disruptants. However, double-strand break formation, which is a key event in the initiation of meiotic DNA recombination, occurred; crossover and noncrossover products were observed in the disruptants, although the amounts of these products were slightly decreased compared with those in wild-type cells. The spores produced by sgs1disruptants showed relatively high viability. The sgs1 spo13 double disruptants sporulated poorly, like the sgs1 disruptants, but spore viability was reduced much more than with either sgs1 or spo13 single disruptants. Disruption of the RED1 or RAD17gene partially alleviated the poor-sporulation phenotype of sgs1 disruptants, indicating that portions of the population of sgs1 disruptants are blocked by the meiotic checkpoint. The poor sporulation of sgs1 disruptants was complemented with a mutated SGS1 gene encoding a protein lacking DNA helicase activity; however, the mutated gene could suppress neither the sensitivity of sgs1 disruptants to methyl methanesulfonate and hydroxyurea nor the mitotic hyperrecombination phenotype of sgs1 disruptants.
ACKNOWLEDGMENTS
We are grateful to A. Sugino, N. Kleckner, H. Ogawa, R. E. Malone, and T. Weinert for providing plasmid DNAs and yeast strains.
This work was supported by grants-in-aid for scientific research and for scientific research on priority areas from the Ministry of Education, Science, Sports and Culture of Japan, health sciences research grants from the Ministry of Health and Welfare of Japan, a grant from the CREST of the JST and the Human Frontier Science Program, and a grant from the Mitsubishi Foundation.