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Sci. Signal., 31 January 2012
Vol. 5, Issue 209, p. ra9
[DOI: 10.1126/scisignal.2002435]

RESEARCH ARTICLES

Editor's Summary

Bypassing TOR
Without target of rapamycin (TOR), cells cannot properly integrate nutrient status with cell growth. In yeast, loss of one of the Tor-encoding genes, TOR2, is lethal. Cardon et al. found that phosphorylation of Ugp1 by the yeast PASK (yPASK) family members rescued the growth defect of a temperature-sensitive tor2 yeast mutant. This rescue involved the formation of a multiprotein complex that activated the guanosine triphosphatase Rho1 and was independent of the well-known function of Ugp1 in supplying glucose for cell wall synthesis. This work defines a pathway that provides a pro-growth signal in the absence of Tor2 and shows that yPASK-phosphorylated Ugp1 is a dual-purpose protein, directing glucose to the periphery for cell wall synthesis and activating Rho1 to promote cell growth.

Citation: C. M. Cardon, T. Beck, M. N. Hall, J. Rutter, PAS Kinase Promotes Cell Survival and Growth Through Activation of Rho1. Sci. Signal. 5, ra9 (2012).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Science Signaling Podcast: 31 January 2012.
C. M. Cardon, J. Rutter, and A. M. VanHook (2012)
Science Signaling 5, pc2
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