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Published online on April 28, 2008
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0801087105


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CELL BIOLOGY
Nuclear translocation of Gln3 in response to nutrient signals requires Golgi-to-endosome trafficking in Saccharomyces cerevisiae

Rekha Puria, Sara A. Zurita-Martinez, and Maria E. Cardenas*

Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710

Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved March 6, 2008 (received for review February 2, 2008)

Abstract

The yeast Saccharomyces cerevisiae has developed specialized mechanisms that enable growth on suboptimal nitrogen sources. Exposure of yeast cells to poor nitrogen sources or treatment with the Tor kinase inhibitor rapamycin elicits activation of Gln3 and transcription of nitrogen catabolite-repressed (NCR) genes whose products function in scavenging and metabolizing nitrogen. Here, we show that mutations in class C and D Vps components, which mediate Golgi-to-endosome vesicle transport, impair nuclear translocation of Gln3, NCR gene activation, and growth in poor nitrogen sources. In nutrient-replete conditions, a significant fraction of Gln3 is peripherally associated with light membranes and partially colocalizes with Vps10-containing foci. These results reveal a role for Golgi-to-endosome vesicular trafficking in TORC1-controlled nuclear translocation of Gln3 and support a model in which Tor-mediated signaling in response to nutrient cues occurs in these compartments. These findings have important implications for nutrient sensing and growth control via mTor pathways in metazoans.

rapamycin action | Tor signaling

Footnotes

Author contributions: R.P. and M.E.C. designed research; R.P., S.A.Z.-M., and M.E.C. performed research; R.P. and S.A.Z.-M. contributed new reagents/analytic tools; R.P., S.A.Z.-M., and M.E.C. analyzed data; and R.P. and M.E.C. wrote the paper.

The authors declare no conflict of interest.

This article is a PNAS Direct Submission.

*To whom correspondence should be addressed. E-mail: carde004{at}mc.duke.edu

© 2008 by The National Academy of Sciences of the USA


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