Repression of transcription by Rgt1 in the absence of glucose requires Std1 and Mth1
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In the yeast Saccharomyces cerevisiae, glucose induces expression of the hexose transporter (HXT) genes by inhibiting the repressor function of the transcription factor Rgt1. We have previously shown that Rgt1 binds to the HXT gene promoters only in the absence of glucose. In the presence of glucose, Rgt1 becomes phosphorylated and is unable to bind to the HXT promoters and repress their transcription. We report that Rgt1 interacts with Std1 and Mth1 in a yeast two-hybrid assay and co-immunoprecipitates with both proteins in vivo only when glucose is absent. In addition, we demonstrate that repression of HXT gene expression by Rgt1 is abolished in the std1 mth1 double mutant. While Rgt1 is normally phosphorylated only in the presence of high concentrations of glucose, it is constitutively modified in the std1 mth1 double mutant. Based on these data, we conclude that, in the absence of glucose, Rgt1 associates with Std1 and Mth1 to repress HXT gene expression.
Keywords.Yeast Glucose HXT Rgt1 Mth1 Std1
We would like to thank Mark Johnston and the members of his laboratory for sharing data prior to publication. We are grateful to Martin Schmidt for providing us with the STD1 and MTH1 strains and plasmids and to Wally Whiteheart for the HA antibody. We thank Bishwa Aryal and Courtney Reynolds for excellent technical assistance.
- Flick KM, Spielewoy N, Guaderrama M, Kalishnikova T, Zhu QZ, Chang H-C, Witternberg C (2003) Grr1-dependent inactivation of Mth1 mediates glucose induced dissociation of Rgt1 from HXT gene promoters. Mol Biol Cell (in press)Google Scholar
- Özcan S, Johnston M (1999) Function and regulation of yeast hexose transporters. Microbiol Mol Biol Rev 63:554–569Google Scholar
- Schmidt MC, McCartney RR, Zhang X, Tillman TS, Solimeo H, Wolf S, Almonte C, Watkins SC (1999) Std1 and Mth1 proteins interact with the glucose sensors to control glucose-regulated gene expression in Saccharomyces cerevisiae. Mol Cell Biol 19:4561–4571Google Scholar