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Article Addendum

Deletion of HOG1 Leads to Osmosensitivity in Starvation-Induced, but not Rapamycin-Dependent Atg8 Degradation and Proteolysis: Further Evidence for Different Regulatory Mechanisms in Yeast Autophagy

Tanja Prick, Michael Thumm, Dieter Häussinger and Stephan vom Dahl

volume 2 | issue 3

July/August/September 2006
Pages: 241 - 243

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The mechanisms of regulation of autophagy are still obscure. In mammalian liver, starvation-induced autophagic proteolysis is regulated by the cellular hydration state in a microtubule- and p38MAPK-dependent way. Recent work shows that in yeast, loss of Hog1, the yeast orthologue of p38MAPK, leads to osmosensitivity of starvation-induced autophagy (Prick et al. Biochem J 2006; 394:153-61), pointing to an evolutionarily conserved mechanism. In this addendum further experiments from hog1delta yeast cells are shown, which support the hypothesis that starvation- and rapamycin-induced autophagy processes differ in their susceptibility to osmotic stress. The potential mechanisms are discussed.

Addendum to:
In Yeast, Loss of Hog1 Leads to Osmosensitivity of Autophagy
T. Prick, M. Thumm, K. Kohrer, D. Haussinger and S. vom Dahl
Biochem J 2006; 394:153-61



We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 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.