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Papers In Press, published online ahead of print May 16, 2001
Wine Research Center, University of British Columbia, Vancouver, BC V6T 1Z4
Corresponding Author: hjjvv{at}interchange.ubc.ca
The GATA-family proteins Gln3p and Gat1p mediate nitrogen catabolite repression (NCR)-sensitive transcription in S. cerevisiae. When cells are cultured with a good nitrogen source (glutamine, ammonia), Gln3p and Gat1p are restricted to the cytoplasm, whereas with a poor nitrogen source (proline), they localize to the nucleus, bind to the GATA sequences of NCR-sensitive gene promoters, and activate transcription. The TOR-signaling cascade and Ure2p participate in regulating the cellular localization of Gln3p and Gat1p. Rapamycin, a Tor protein inhibitor, like growth with a poor nitrogen source, promotes nuclear localization of Gln3p and Gat1p. gln3 and ure2 deletion mutants are partially resistant and hyper-sensitive to growth inhibition by rapamycin, respectively. We show that a vid30 deletion is more rapamycin-sensitive than wild type but less so than a ure2 deletion. VID30 expression is modestly NCR-sensitive, responsive to deletion of URE2, and greatly increases in low ammonia medium. Patterns of gene expression in a vid30 deletion suggest that the Vid30p function shifts the balance of nitrogen metabolism towards the production of glutamate especially when cells are grown in low ammonia. CAN1, DAL4, DAL5, MEP2, DAL1, DAL80, and GDH3 transcription is down regulated by Vid30p function with proline as nitrogen source. An effect, however, that could easily be indirect.
J. Biol. Chem, 10.1074/jbc.M102280200
Submitted on March 14, 2001
Revised on May 16, 2001
Accepted on May 16, 2001
Ammonia regulates VID30 expression and Vid30p function shifts nitrogen metabolism towards glutamate formation especially when Saccharomyces cerevisiae is grown in low concentrations of ammonia
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