The Emerging Roles of mTORC1 in Macromanaging Autophagy.
Identifieur interne : 000207 ( Main/Exploration ); précédent : 000206; suivant : 000208The Emerging Roles of mTORC1 in Macromanaging Autophagy.
Auteurs : Akpedje S. Dossou [États-Unis] ; Alakananda Basu [États-Unis]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
Autophagy is a process of self-degradation that enables the cell to survive when faced with starvation or stressful conditions. The mechanistic target of rapamycin (mTOR), also known as the mammalian target of rapamycin, plays a critical role in maintaining a balance between cellular anabolism and catabolism. mTOR complex 1 (mTORC1) was unveiled as a master regulator of autophagy since inhibition of mTORC1 was required to initiate the autophagy process. Evidence has emerged in recent years to indicate that mTORC1 also directly regulates the subsequent steps of the autophagy process, including the nucleation, autophagosome elongation, autophagosome maturation and termination. By phosphorylating select protein targets of the autophagy core machinery and/or their regulators, mTORC1 can alter their functions, increase their proteasomal degradation or modulate their acetylation status, which is a key switch of the autophagy process. Moreover, it phosphorylates and alters the subcellular localization of transcription factors to suppress the expression of genes needed for autophagosome formation and lysosome biogenesis. The purpose of this review article is to critically analyze current literatures to provide an integrated view of how mTORC1 regulates various steps of the autophagy process.
DOI: 10.3390/cancers11101422
PubMed: 31554253
PubMed Central: PMC6826502
Affiliations:
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Dossou</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Akpedje.Dossou@my.unthsc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Basu, Alakananda" sort="Basu, Alakananda" uniqKey="Basu A" first="Alakananda" last="Basu">Alakananda Basu</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Alakananda.basu@unthsc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author></analytic><series><title level="j">Cancers</title><idno type="ISSN">2072-6694</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is a process of self-degradation that enables the cell to survive when faced with starvation or stressful conditions. The mechanistic target of rapamycin (mTOR), also known as the mammalian target of rapamycin, plays a critical role in maintaining a balance between cellular anabolism and catabolism. mTOR complex 1 (mTORC1) was unveiled as a master regulator of autophagy since inhibition of mTORC1 was required to initiate the autophagy process. Evidence has emerged in recent years to indicate that mTORC1 also directly regulates the subsequent steps of the autophagy process, including the nucleation, autophagosome elongation, autophagosome maturation and termination. By phosphorylating select protein targets of the autophagy core machinery and/or their regulators, mTORC1 can alter their functions, increase their proteasomal degradation or modulate their acetylation status, which is a key switch of the autophagy process. Moreover, it phosphorylates and alters the subcellular localization of transcription factors to suppress the expression of genes needed for autophagosome formation and lysosome biogenesis. The purpose of this review article is to critically analyze current literatures to provide an integrated view of how mTORC1 regulates various steps of the autophagy process.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">31554253</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Print">2072-6694</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>10</Issue><PubDate><Year>2019</Year><Month>Sep</Month><Day>24</Day></PubDate></JournalIssue><Title>Cancers</Title><ISOAbbreviation>Cancers (Basel)</ISOAbbreviation></Journal><ArticleTitle>The Emerging Roles of mTORC1 in Macromanaging Autophagy.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E1422</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/cancers11101422</ELocationID><Abstract><AbstractText>Autophagy is a process of self-degradation that enables the cell to survive when faced with starvation or stressful conditions. The mechanistic target of rapamycin (mTOR), also known as the mammalian target of rapamycin, plays a critical role in maintaining a balance between cellular anabolism and catabolism. mTOR complex 1 (mTORC1) was unveiled as a master regulator of autophagy since inhibition of mTORC1 was required to initiate the autophagy process. Evidence has emerged in recent years to indicate that mTORC1 also directly regulates the subsequent steps of the autophagy process, including the nucleation, autophagosome elongation, autophagosome maturation and termination. By phosphorylating select protein targets of the autophagy core machinery and/or their regulators, mTORC1 can alter their functions, increase their proteasomal degradation or modulate their acetylation status, which is a key switch of the autophagy process. Moreover, it phosphorylates and alters the subcellular localization of transcription factors to suppress the expression of genes needed for autophagosome formation and lysosome biogenesis. The purpose of this review article is to critically analyze current literatures to provide an integrated view of how mTORC1 regulates various steps of the autophagy process.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dossou</LastName><ForeName>Akpedje S</ForeName><Initials>AS</Initials><Identifier Source="ORCID">0000-0002-9844-8860</Identifier><AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Akpedje.Dossou@my.unthsc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Basu</LastName><ForeName>Alakananda</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-1656-0788</Identifier><AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. 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