Rst1 and Rst2 are required for the a/α diploid cell type in yeast

Abstract

In the budding yeast Saccharomyces cerevisiae, the preservation of the mating competent haploid (a or α) and the mating incompetent diploid (a/α) is necessary to prevent aneuploidy. Once haploid cells respond to pheromone, the mating-specific signal transduction pathway is activated, and the MAP kinase Fus3 phosphorylates two specific repressor proteins Rst1 and Rst2 (also known as Dig1 and Dig2) to promote Ste 12-dependent transcription of mating-specific genes. In contrast, diploid cells cannot mate because genes that encode components of the mating pathway are repressed through the combined action of the Mata1-Matα2 and Matα2-Mcm1 repressors. Surprisingly, repression of Ste 12 by Rst1 and Rst2 is essential for diploid sterility. Homozygous deletion of both RST1 and RST2 (rst-) causes a/α diploid cells constitutively to express a-specific genes and mate preferentially as a-cells. This phenotype is sensitive to Ste 12 dosage, as removal of one copy of STE 12 completely reduces the ectopic activation of a-specific genes. The Matα2-Mcm 1 complex, which normally represses a-specific genes, is defective in rst- diploids because Matα2 is destabilized in rst- diploids, possibly as a consequence of its relocalization from the nucleus to the cytoplasm. This study finds that Rst1 and Rst2 are necessary for the a/α diploid cell type. Rst1 and Rst2 are required in order to prevent the amplification of a robust Ste 12 transcriptional programme that appears to over-ride Matα2-dependent repression of haploid and a-specific genes.