The Nem1/Spo7–Pah1/lipin axis is required for autophagy induction after TORC1 inactivation
Autophagy is a process that requires intense membrane remodeling and consumption. The nutrient‐responsive TORC1 (target of rapamycin complex 1) kinase regulates autophagy. However, how TORC1 controls autophagy via lipid/membrane biogenesis is unknown. TORC1 regulates the function of yeast phosphatid...
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Published in | The FEBS journal Vol. 285; no. 10; pp. 1840 - 1860 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
Blackwell Publishing Ltd
01.05.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Autophagy is a process that requires intense membrane remodeling and consumption. The nutrient‐responsive TORC1 (target of rapamycin complex 1) kinase regulates autophagy. However, how TORC1 controls autophagy via lipid/membrane biogenesis is unknown. TORC1 regulates the function of yeast phosphatidate phosphatase lipin Pah1 via the Nem1/Spo7 phosphatase complex. Here, we show that the Nem1/Spo7–Pah1 axis is required for autophagy induction after TORC1 inactivation and survival during starvation. Furthermore, this axis was critical for nucleophagy (both micronucleophagy and macronucleophagy) and was required for proper localization of micronucleophagy factor Nvj1 and macronucleophagy receptor Atg39. This study indicated that the Nem1/Spo7–Pah1 axis controlled by TORC1 is a critical branch for autophagy induction in nutrient starvation conditions.
Nutrient starvation and TORC1 (target of rapamycin complex 1) inactivation promotes autophagy induction via the Nem1/Spo7–Pah1/lipin axis that is required for production of diacylglycerol (DAG) production and then triacylglycerol (TAG). This axis is critical for nucleophagy (both micronucleophagy and macronucleophagy) and is required for proper localization of micronucleophagy factor Nvj1 and macronucleophagy receptor Atg39. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1742-464X 1742-4658 |
DOI: | 10.1111/febs.14448 |