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The Yeast ARD] Gene Product Is Required for Repression of Cryptic Mating-Type Information at the HML Locust

Mutations in the ARD1 gene prevent yeast cells from displaying GI-specific growth arrest in response to nitrogen deprivation and cause MATa haploids (but not MATa haploids) to be mating defective. Analysis of cell type-specific gene expression by examination of RNA transcripts and measurement of i-galactosidase activity from yeast gene-lacZ fusions demonstrated that the mating defect of MATa ardi mutants was due to an inability to express genes required by MATa cells for the mating process. The lack of mating-specific gene expression in MATa cells was found to be due solely to derepression of the normally silent a information at the HML locus. The cryptic a information at the HMR locus was only very slightly derepressed in ardi mutants, to a level insufficient to affect the mating efficiency of MATa cells. The preferential elevation of expression from HML over HMR was also observed in ardi mutants which contained the alternate arrangement of a information at HML and a information at HMR. Hence, the effect of the ardl mutation was position specific (rather than information specific). Although the phenotype of ardl mutants resembled that of cells with mutations in the SIR) gene, both genetic and biochemical findings indicated that ARD1 control of HML expression was independent of the regulation imposed by SIR) and the other SIR genes. These results suggest that the ARDi gene encodes a protein product that acts, directly or indirectly, at the HML locus to repress its expression and, by analogy, may control expression of other genes involved in monitoring nutritional conditions. The yeast Saccharomyces cerevisiae can exist as one