Loss of IRA2 suppresses the growth defect on low glucose caused by the snf3 mutation in Saccharomyces cerevisiae


  • Present address: George Theodoris, Arcadia Bio Sciences, Davis, CA 95616, USA.

  • Editor: Terrance Cooper

Correspondence: Linda Bisson, One Shields Avenue, Davis, CA 95616-8749, USA. Tel.: +1 530 752 3835; fax: +1 530 752 0382; e-mail: lfbisson@ucdavis.edu


SNF3 encodes a low-glucose sensor in Saccharomyces cerevisiae that regulates the expression of a subset of hexose transporter genes. Deletion of SNF3 prevents rapid adaptation to low glucose concentration. Novel spontaneous suppressor mutants of the snf3Δ phenotype were isolated. The mutations isolated fell into one of two groups: those that increase the expression of transporters regulated by Snf3p, and those that show no detectable effect on the regulation of these genes. The physiologic role of one mutation, rgg2 (restoration of growth on glucose), that did not affect HXT gene expression was assessed by transcriptome analysis. Genes involved in glycogen metabolism and cAMP pathways were affected by the rgg2 mutation, suggesting a cellular role as a regulatory protein. Attempts to clone the wild-type RGG2 allele were unsuccessful. The glycogen phenotype and genetic crossing allowed rgg2 to be identified as an allele of the IRA2 gene. Suppression of the snf3 mutant phenotype by deletion of IRA2 was confirmed. A possible mechanism of the suppression of the snf3 growth defect by mutation of ira2 is discussed.