Stress-response transcription factors Msn2 and Msn4 couple TORC2-Ypk1 signaling and mitochondrial respiration to ATG8 gene expression and autophagy.
Identifieur interne : 000740 ( Main/Exploration ); précédent : 000739; suivant : 000741Stress-response transcription factors Msn2 and Msn4 couple TORC2-Ypk1 signaling and mitochondrial respiration to ATG8 gene expression and autophagy.
Auteurs : Ariadne Vlahakis [États-Unis] ; Nerea Lopez Muniozguren [États-Unis] ; Ted Powers [États-Unis]Source :
- Autophagy [ 1554-8635 ] ; 2017.
Descripteurs français
- KwdFr :
- Acides aminés (déficit), Autophagie (génétique), Complexe-2 cible mécanistique de la rapamycine (métabolisme), Facteurs de transcription (métabolisme), Famille de la protéine-8 associée à l'autophagie (génétique), Glycogen Synthase Kinase 3 (métabolisme), Mitochondries (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines de liaison à l'ADN (métabolisme), Protéines de répression (métabolisme), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Stress physiologique (génétique), Transduction du signal (MeSH).
- MESH :
- déficit : Acides aminés.
- génétique : Autophagie, Famille de la protéine-8 associée à l'autophagie, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae, Stress physiologique.
- métabolisme : Complexe-2 cible mécanistique de la rapamycine, Facteurs de transcription, Glycogen Synthase Kinase 3, Mitochondries, Protéines de Saccharomyces cerevisiae, Protéines de liaison à l'ADN, Protéines de répression, Saccharomyces cerevisiae.
- Régulation de l'expression des gènes fongiques, Transduction du signal.
English descriptors
- KwdEn :
- Amino Acids (deficiency), Autophagy (genetics), Autophagy-Related Protein 8 Family (genetics), DNA-Binding Proteins (metabolism), Gene Expression Regulation, Fungal (MeSH), Glycogen Synthase Kinase 3 (metabolism), Mechanistic Target of Rapamycin Complex 2 (metabolism), Mitochondria (metabolism), Repressor Proteins (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Stress, Physiological (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , deficiency : Amino Acids.
- genetics : Autophagy, Autophagy-Related Protein 8 Family, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Stress, Physiological.
- chemical , metabolism : DNA-Binding Proteins, Glycogen Synthase Kinase 3, Mechanistic Target of Rapamycin Complex 2, Mitochondria, Repressor Proteins, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Transcription Factors.
- Gene Expression Regulation, Fungal, Signal Transduction.
Abstract
Macroautophagy/autophagy is a starvation and stress-induced catabolic process critical for cellular homeostasis and adaptation. Several Atg proteins are involved in the formation of the autophagosome and subsequent degradation of cytoplasmic components, a process termed autophagy flux. Additionally, the expression of several Atg proteins, in particular Atg8, is modulated transcriptionally, yet the regulatory mechanisms involved remain poorly understood. Here we demonstrate that the AGC kinase Ypk1, target of the rapamycin-insensitive TORC2 signaling pathway, controls ATG8 expression by repressing the heterodimeric Zinc-finger transcription factors Msn2 and Msn4. We find that Msn2 and Msn4 promote ATG8 expression downstream of the histone deacetylase complex (HDAC) subunit Ume6, a previously identified negative regulator of ATG8 expression. Moreover, we demonstrate that TORC2-Ypk1 signaling is functionally linked to distinct mitochondrial respiratory complexes. Surprisingly, we find that autophagy flux during amino acid starvation is also dependent upon Msn2-Msn4 activity, revealing a broad role for these transcription factors in the autophagy response.
DOI: 10.1080/15548627.2017.1356949
PubMed: 29198169
PubMed Central: PMC5788474
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Several Atg proteins are involved in the formation of the autophagosome and subsequent degradation of cytoplasmic components, a process termed autophagy flux. Additionally, the expression of several Atg proteins, in particular Atg8, is modulated transcriptionally, yet the regulatory mechanisms involved remain poorly understood. Here we demonstrate that the AGC kinase Ypk1, target of the rapamycin-insensitive TORC2 signaling pathway, controls ATG8 expression by repressing the heterodimeric Zinc-finger transcription factors Msn2 and Msn4. We find that Msn2 and Msn4 promote ATG8 expression downstream of the histone deacetylase complex (HDAC) subunit Ume6, a previously identified negative regulator of ATG8 expression. Moreover, we demonstrate that TORC2-Ypk1 signaling is functionally linked to distinct mitochondrial respiratory complexes. Surprisingly, we find that autophagy flux during amino acid starvation is also dependent upon Msn2-Msn4 activity, revealing a broad role for these transcription factors in the autophagy response.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29198169</PMID><DateCompleted><Year>2019</Year><Month>06</Month><Day>04</Day></DateCompleted><DateRevised><Year>2019</Year><Month>06</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>11</Issue><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>Stress-response transcription factors Msn2 and Msn4 couple TORC2-Ypk1 signaling and mitochondrial respiration to ATG8 gene expression and autophagy.</ArticleTitle><Pagination><MedlinePgn>1804-1812</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2017.1356949</ELocationID><Abstract><AbstractText>Macroautophagy/autophagy is a starvation and stress-induced catabolic process critical for cellular homeostasis and adaptation. Several Atg proteins are involved in the formation of the autophagosome and subsequent degradation of cytoplasmic components, a process termed autophagy flux. Additionally, the expression of several Atg proteins, in particular Atg8, is modulated transcriptionally, yet the regulatory mechanisms involved remain poorly understood. Here we demonstrate that the AGC kinase Ypk1, target of the rapamycin-insensitive TORC2 signaling pathway, controls ATG8 expression by repressing the heterodimeric Zinc-finger transcription factors Msn2 and Msn4. We find that Msn2 and Msn4 promote ATG8 expression downstream of the histone deacetylase complex (HDAC) subunit Ume6, a previously identified negative regulator of ATG8 expression. Moreover, we demonstrate that TORC2-Ypk1 signaling is functionally linked to distinct mitochondrial respiratory complexes. Surprisingly, we find that autophagy flux during amino acid starvation is also dependent upon Msn2-Msn4 activity, revealing a broad role for these transcription factors in the autophagy response.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vlahakis</LastName><ForeName>Ariadne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>a Department of Molecular and Cellular Biology , College of Biological Sciences, University of California, Davis , Davis , CA , USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b Department of Pathology , University of California, San Francisco , San Francisco , CA , USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lopez Muniozguren</LastName><ForeName>Nerea</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>a Department of Molecular and Cellular Biology , College of Biological Sciences, University of California, Davis , Davis , CA , 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MajorTopicYN="N">Amino Acids</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071190" MajorTopicYN="N">Autophagy-Related Protein 8 Family</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="Y">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D038362" MajorTopicYN="N">Glycogen Synthase Kinase 3</DescriptorName><QualifierName UI="Q000378" 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