Cdc14 Phosphatase Promotes TORC1-Regulated Autophagy in Yeast
Cdc14 protein phosphatase is critical for late mitosis progression in budding yeast, although its orthologs in other organisms, including mammalian cells, function as stress-responsive phosphatases. We found herein unexpected roles of Cdc14 in autophagy induction after nutrient starvation and target...
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Published in | Journal of molecular biology Vol. 430; no. 11; pp. 1671 - 1684 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Ltd
25.05.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Cdc14 protein phosphatase is critical for late mitosis progression in budding yeast, although its orthologs in other organisms, including mammalian cells, function as stress-responsive phosphatases. We found herein unexpected roles of Cdc14 in autophagy induction after nutrient starvation and target of rapamycin complex 1 (TORC1) kinase inactivation. TORC1 kinase phosphorylates Atg13 to repress autophagy under nutrient-rich conditions, but if TORC1 becomes inactive upon nutrient starvation or rapamycin treatment, Atg13 is rapidly dephosphorylated and autophagy is induced. Cdc14 phosphatase was required for optimal Atg13 dephosphorylation, pre-autophagosomal structure formation, and autophagy induction after TORC1 inactivation. In addition, Cdc14 was required for sufficient induction of ATG8 and ATG13 expression. Moreover, Cdc14 activation provoked autophagy even under normal conditions. This study identified a novel role of Cdc14 as the stress-responsive phosphatase for autophagy induction in budding yeast.
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•Yeast Cdc14 protein phosphatase is required for optimal Atg13 dephosphorylation, pre-autophagosomal structure formation, and autophagy induction after TORC1 inactivation.•Cdc14 is required for sufficient induction of ATG8 and ATG13 expression.•Cdc14 activation provokes autophagy even in normal conditions. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-2836 1089-8638 |
DOI: | 10.1016/j.jmb.2018.04.007 |