Components of the Vid30c are needed for the rapamycin-induced degradation of the high-affinity hexose transporter Hxt7p in Saccharomyces cerevisiae

Chris Snowdon, Chris Hlynialuk, George Van Der Merwe

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)204-216
Number of pages13
JournalFEMS yeast research
Volume8
Issue number2
DOIs
StatePublished - Mar 2008

Keywords

  • Nitrogen starvation
  • Rapamycin-induced Hxt7p turnover
  • Saccharomyces cerevisiae
  • Vid28p and Vid30p
  • Vid30c

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