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Components of the Vid30c are needed for the rapamycin-induced degradation of the high-affinity hexose transporter Hxt7p in Saccharomyces cerevisiae
Article first published online: 6 NOV 2007
DOI: 10.1111/j.1567-1364.2007.00327.x
© 2007 Federation of European Microbiological Societies
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How to Cite
Snowdon, C., Hlynialuk, C. and Van Der Merwe, G. (2008), Components of the Vid30c are needed for the rapamycin-induced degradation of the high-affinity hexose transporter Hxt7p in Saccharomyces cerevisiae. FEMS Yeast Research, 8: 204–216. doi: 10.1111/j.1567-1364.2007.00327.x
Publication History
- Issue published online: 6 NOV 2007
- Article first published online: 6 NOV 2007
- Received 13 June 2007; revised 20 August 2007; accepted 4 September 2007.First published online 8 November 2007.
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Keywords:
- Vid28p and Vid30p;
- rapamycin-induced Hxt7p turnover;
- nitrogen starvation;
- Vid30c;
- Saccharomyces cerevisiae
Abstract
Saccharomyces cerevisiae adapts to changing nutrient conditions by regulating its genome-wide transcription profile and cell-wide protein complement in correlation with the reigning nutrient conditions. The target of rapamycin (TOR) signalling pathway is one of the major control mechanisms within the cell that facilitates these changes. The transcription, intracellular trafficking, and protein turnover of nutrient transporters, including the hexose transporter proteins (Hxts), are regulated in response to nutrient conditions. The Vid and Gid proteins facilitate the nutrient-dependent degradation of the gluconeogenic enzymes FBPase and Mdh2p when glucose-starved cells are replenished with glucose. Three members of the VID and GID gene families, VID30/GID1, GID2, and VID28/GID5 are needed for the rapamycin or nitrogen starvation-induced degradation of the high-affinity hexose transporter Hxt7p is shown here. In addition, evidence that the functions of several Vid and Gid proteins are in close relation to the TOR signalling pathway is provided.