Open AccessDDSE: downstream targets of the SNF3 signal transduction pathway
Author(s) -
Theodoris George,
Bisson Linda F
Publication year - 2001
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2001.tb10585.x
Subject(s) - repressor , snf3 , mutant , lac repressor , biology , promoter , gene , activator (genetics) , microbiology and biotechnology , derepression , gene expression , psychological repression , saccharomyces cerevisiae , genetics
Mutations in the yeast SNF3 gene affect glucose sensing and snf3 mutants show defective growth on glucose. DNA sequence dependent suppressing elements (DDSEs) are regions located in the promoters of yeast glucose transporter ( HXT ) genes that when present in high copy suppress the snf3 growth defect. Here we provide evidence that the multicopy DDSE suppression is due to the titration of the Rgt1p transcriptional repressor. The DDSE region from HXT4 was found to function as a UAS sequence rendering a UAS gal ‐less LacZ gene fused to the GAL1 promoter responsive to glucose induction. Expression mediated by the UAS DDSE was dependent upon the presence of Snf3p. Expression was elevated to a high level in an rgt1 mutant in the absence of Snf3p suggesting that this DDSE region contains binding sites for the Rgt1p transcriptional repressor/activator. The UAS DDSE led to expression in a grr1 mutant background, which confers a defect in inactivation of Rgt1p, as predicted from the model. The presence of tandem repeats of the putative Rgt1p binding site gave results similar to those of the DDSE, suggesting that loss of repression is due to the presence of Rgt1p footprint in the multicopy DDSE.