RAS2 of Saccharomyces cerevisiae is required for gluconeogenic growth and proper response to nutrient limitation.

Abstract

S. cerevisiae contains 2 genes with remarkable homology to members of the ras oncogene family. These 2 genes, RAS1 and RAS2, constitute an essential gene family since spores with disruptions of both genes fail to grow. Strains containing RAS2 disruptions have 3 distinct phenotypes. First, they fail to grow efficiently on nonfermentable carbon sources. Second, they hyperaccumulate the storage carbohydrates glycogen and trehalose. Third, diploid cells homozygous for the RAS2 disruptions sporulate on rich media. Extragenic suppressors were isolated that suppress the gluconeogenic defect. These suppressors fall into at least 3 complementation groups, mutations in 2 of which bypass the normal requirement of RAS for cell viability, allowing cells containing neither RAS gene to grow. The phenotype of the RAS2 mutant and extragenic suppressors implicate RAS with some function in the normal response to nutrient limitation.