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Title: Mitochondrial Complex I Activity Is Required for Maximal Autophagy
Author: Thomas, Hala Elnakat
Zhang, Yu
Stefely, Jonathan A.
Veiga, Sonia R.
Thomas, George
Kozma, Sara C.
Mercer, Carol A.
Keywords: Autofàgia
Issue Date: 28-Aug-2018
Publisher: Cell Press
Abstract: Cells adapt to nutrient and energy deprivation by inducing autophagy, which is regulated by the mammalian target of rapamycin (mTOR) and AMP-activated protein kinases (AMPKs). We found that cell metabolism significantly influences the ability to induce autophagy, with mitochondrial complex I function being an important factor in the initiation, amplitude, and duration of the response. We show that phenformin or genetic defects in complex I suppressed autophagy induced by mTOR inhibitors, whereas autophagy was enhanced by strategies that increased mitochondrial metabolism. We report that mTOR inhibitors significantly increased select phospholipids and mitochondrial-associated membranes (MAMs) in a complex I-dependent manner. We attribute the complex I autophagy defect to the inability to increase MAMs, limiting phosphatidylserine decarboxylase (PISD) activity and mitochondrial phosphatidylethanolamine (mtPE), which support autophagy. Our data reveal the dynamic and metabolic regulation of autophagy.
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It is part of: Cell Reports, 2018, vol. 24, num. 9, p. 2404–2417
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Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

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