A novel Rtg2p activity regulates nitrogen catabolism in yeast

The inactivity of Ure2p, caused by either a ure2 mutation or the presence of the [URE3] prion, increases DAL5 transcription and thus enables Saccharomyces cerevisiae to take up ureidosuccinate (USA+). Rtg2p regulates transcription of glutamate-repressible genes by facilitation of the nuclear entry of the Rtg1 and Rtg3 proteins. We find that rtg2Δ cells take up USA even without the presence of [URE3]. Thus, the USA+ phenotype of rtg2Δ strains is not the result generation of the [URE3] prion but is a regulatory effect. Because rtg1Δ or rtg3Δ mutations or the presence of glutamate do not produce the USA+ phenotype, this is a novel function of Rtg2p. The USA+ phenotype of rtg2Δ strains depends on GLN3, is caused by overexpression of DAL5, and is blocked by mks1Δ, but not by overexpression of Ure2p. These characteristics suggest that Rtg2p acts in the upstream part of the nitrogen catabolism regulation pathway.