Open AccessMutations in GSF1 and GSF2 Alter Glucose Signaling in Saccharomyces cerevisiae
Author(s) -
Peter Sherwood,
Marian Carlson
Publication year - 1997
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1093/genetics/147.2.557
Subject(s) - complementation , biology , saccharomyces cerevisiae , psychological repression , gene , mutant , snf3 , transcription factor , genetics , phenotype , transcription (linguistics) , protein kinase a , kinase , gene expression , linguistics , philosophy
One function of the Saccharomyces cerevisiae Snf1 protein kinase is to relieve glucose repression of SUC, GAL, and other genes in response to glucose depletion. To identify genes that regulate Snf1 kinase activity, we have selected mutants that inappropriately express a SUC2promoter::HIS3 gene fusion when grown in glucose and that require Snf1 function for this phenotype. Mutations representing two new complementation groups (gsf1 and gsf2) were isolated. gsf1 mutations affect two distinct responses to glucose: the Snf1-regulated glucose repression of SUC2 and GAL10 transcription and the Snf1-independent induction by glucose of HXT1 transcription. gsf2 mutations relieve glucose repression of SUC2 and GAL10 transcription and, in combination with snf1 delta, cause an extreme slow growth phenotype. The GSF2 gene was cloned by complementation of the gsf2-1 snf1 delta slow growth phenotype and encodes a previously uncharacterized 46kD protein.