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Rapamycin bypasses vesicle-mediated signaling events to activate Gln3 in Saccharomyces cerevisiae

Rekha Puria and Maria E. Cardenas

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Growth of Saccharomyces cerevisiae in poor nitrogen sources or exposure to the Tor inhibitor rapamycin results in expression of the nitrogen catabolite repressed (NCR) genes whose products are involved in scavenging and metabolizing nitrogen. The NCR genes are regulated by the GATA-like transactivators Gln3 and Gat1, which are thought to be under control of the rapamycin-sensitive Tor complex 1 (TORC1). We have recently shown that Gln3 nuclear translocation in response to nitrogen source quality but not in response to rapamycin requires Golgi to endosome trafficking. These and previous findings that several TORC1 components localize to low density endomembranes are discussed in a model that underscores a prominent role for the vesicular trafficking system in facilitating molecular interactions in response to nitrogen source. In addition, these findings have important implications for Tor signaling and rapamycin mechanism of action, both in yeast and in metazoans.

Authors

Rekha Puria

Duke University Medical Center

Maria E. Cardenas

Duke University Medical Center

This is an open-access article

 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.