Ammonia regulates VID30 expression and Vid30p function shifts nitrogen metabolism toward glutamate formation especially when Saccharomyces cerevisiaeis grown in low concentrations of ammonia

The GATA family proteins Gln3p and Gat1p mediate nitrogen catabolite repres sion (NCR)-sensitive transcription in Saccharomyces cerevisiae. When cells are cultured with a good nitrogen source (glutamine, ammonia), Gln3p and Ga t1p are restricted to the cytoplasm, whereas with a poor nitrogen source (p roline), they localize to the nucleus, bind to the GATA sequences of NCR-se nsitive gene promoters, and activate transcription. The target of rapamycin -signaling cascade and Ure2p participate in regulating the cellular localiz ation of Gln3p and Gat1p. Rapamycin, a Tor protein inhibitor, like growth w ith a poor nitrogen source, promotes nuclear localization of Gln3p and Gat1 p. gln3 Delta and ure2 Delta mutants are partially resistant and hypersensi tive to growth inhibition by rapamycin, respectively. We show that a vid30 Delta is more rapamycin-sensitive than wild type but less so than a ure2 De lta. VID30 expression is modestly NCR-sensitive, responsive to deletion of URE2, and greatly increases in low ammonia medium. Patterns of gene express ion in a vid30 Delta suggest that the Vid30p function shifts the balance of nitrogen metabolism toward the production of glutamate, especially when ce lls are grown in low ammonia. CAN1, DAL4, DAL5, MEP2, DAL1, DAL80, and GDH3 transcription is down-regulated by Vid30p function with proline as the nit rogen source. An effect, however, that could easily be indirect.