FEBS Letters
Volume 581, Issue 17 , Pages 3230-3234, 10 July 2007

Biochemical evidence for glucose-independent induction of HXT expression in Saccharomyces cerevisiae

Edited by Ivan Sadowski

Mississippi Functional Genomics Network, Department of Biological Sciences, The University of Southern Mississippi, 118 College Dr., Hattiesburg, MS 39406, USA

Received 15 April 2007; received in revised form 11 June 2007; accepted 12 June 2007. published online 19 June 2007.

Abstract 

The yeast glucose sensors Rgt2 and Snf3 generate a signal in response to glucose that leads to degradation of Mth1 and Std1, thereby relieving repression of Rgt1-repressed genes such as the glucose transporter genes (HXT). Mth1 and Std1 are degraded via the Yck1/2 kinase-SCFGrr1-26S proteasome pathway triggered by the glucose sensors. Here, we show that RGT2-1 promotes ubiquitination and subsequent degradation of Mth1 and Std1 regardless of the presence of glucose. Site-specific mutagenesis reveals that the conserved lysine residues of Mth1 and Std1 might serve as attachment sites for ubiquitin, and that the potential casein kinase (Yck1/2) sites of serine phosphorylation might control their ubiquitination. Finally, we show that active Snf1 protein kinase in high glucose prevents degradation of Mth1 and Std1.

Abbreviations: SCF, Skp1p-Cullin-F-box protein, GFP, green fluorescent protein

Keywords: HXT, Mth1, Std1, Degradation, RGT2-1, SNF3-1

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PII: S0014-5793(07)00661-8

doi:10.1016/j.febslet.2007.06.013

FEBS Letters
Volume 581, Issue 17 , Pages 3230-3234, 10 July 2007