TORC1 signaling regulates cytoplasmic pH through Sir2 in yeast.
Identifieur interne : 000035 ( Main/Exploration ); précédent : 000034; suivant : 000036TORC1 signaling regulates cytoplasmic pH through Sir2 in yeast.
Auteurs : Mayur Nimbadas Devare [Corée du Sud] ; Yeong Hyeock Kim [Corée du Sud] ; Joohye Jung [Corée du Sud] ; Woo Kyu Kang [Corée du Sud] ; Ki-Sun Kwon [Corée du Sud] ; Jeong-Yoon Kim [Corée du Sud]Source :
- Aging cell [ 1474-9726 ] ; 2020.
Abstract
Glucose controls the phosphorylation of silent information regulator 2 (Sir2), a NAD+ -dependent protein deacetylase, which regulates the expression of the ATP-dependent proton pump Pma1 and replicative lifespan (RLS) in yeast. TORC1 signaling, which is a central regulator of cell growth and lifespan, is regulated by glucose as well as nitrogen sources. In this study, we demonstrate that TORC1 signaling controls Sir2 phosphorylation through casein kinase 2 (CK2) to regulate PMA1 expression and cytoplasmic pH (pHc) in yeast. Inhibition of TORC1 signaling by either TOR1 deletion or rapamycin treatment decreased PMA1 expression, pHc, and vacuolar pH, whereas activation of TORC1 signaling by expressing constitutively active GTR1 (GTR1Q65L) resulted in the opposite phenotypes. Deletion of SIR2 or expression of a phospho-mutant form of SIR2 increased PMA1 expression, pHc, and vacuolar pH in the tor1Δ mutant, suggesting a functional interaction between Sir2 and TORC1 signaling. Furthermore, deletion of TOR1 or KNS1 encoding a LAMMER kinase decreased the phosphorylation level of Sir2, suggesting that TORC1 signaling controls Sir2 phosphorylation. It was also found that Sit4, a protein phosphatase 2A (PP2A)-like phosphatase, and Kns1 are required for TORC1 signaling to regulate PMA1 expression and that TORC1 signaling and the cyclic AMP (cAMP)/protein kinase A (PKA) pathway converge on CK2 to regulate PMA1 expression through Sir2. Taken together, these findings suggest that TORC1 signaling regulates PMA1 expression and pHc through the CK2-Sir2 axis, which is also controlled by cAMP/PKA signaling in yeast.
DOI: 10.1111/acel.13151
PubMed: 32449834
PubMed Central: PMC7294778
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Chungnam National University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Yeong Hyeock" sort="Kim, Yeong Hyeock" uniqKey="Kim Y" first="Yeong Hyeock" last="Kim">Yeong Hyeock Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Jung, Joohye" sort="Jung, Joohye" uniqKey="Jung J" first="Joohye" last="Jung">Joohye Jung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Kang, Woo Kyu" sort="Kang, Woo Kyu" uniqKey="Kang W" first="Woo Kyu" last="Kang">Woo Kyu Kang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Kwon, Ki Sun" sort="Kwon, Ki Sun" uniqKey="Kwon K" first="Ki-Sun" last="Kwon">Ki-Sun Kwon</name><affiliation wicri:level="1"><nlm:affiliation>Aging Intervention Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Aging Intervention Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Jeong Yoon" sort="Kim, Jeong Yoon" uniqKey="Kim J" first="Jeong-Yoon" last="Kim">Jeong-Yoon Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author></analytic><series><title level="j">Aging cell</title><idno type="eISSN">1474-9726</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glucose controls the phosphorylation of silent information regulator 2 (Sir2), a NAD<sup>+</sup> -dependent protein deacetylase, which regulates the expression of the ATP-dependent proton pump Pma1 and replicative lifespan (RLS) in yeast. TORC1 signaling, which is a central regulator of cell growth and lifespan, is regulated by glucose as well as nitrogen sources. In this study, we demonstrate that TORC1 signaling controls Sir2 phosphorylation through casein kinase 2 (CK2) to regulate PMA1 expression and cytoplasmic pH (pHc) in yeast. Inhibition of TORC1 signaling by either TOR1 deletion or rapamycin treatment decreased PMA1 expression, pHc, and vacuolar pH, whereas activation of TORC1 signaling by expressing constitutively active GTR1 (GTR1Q65L) resulted in the opposite phenotypes. Deletion of SIR2 or expression of a phospho-mutant form of SIR2 increased PMA1 expression, pHc, and vacuolar pH in the tor1Δ mutant, suggesting a functional interaction between Sir2 and TORC1 signaling. Furthermore, deletion of TOR1 or KNS1 encoding a LAMMER kinase decreased the phosphorylation level of Sir2, suggesting that TORC1 signaling controls Sir2 phosphorylation. It was also found that Sit4, a protein phosphatase 2A (PP2A)-like phosphatase, and Kns1 are required for TORC1 signaling to regulate PMA1 expression and that TORC1 signaling and the cyclic AMP (cAMP)/protein kinase A (PKA) pathway converge on CK2 to regulate PMA1 expression through Sir2. Taken together, these findings suggest that TORC1 signaling regulates PMA1 expression and pHc through the CK2-Sir2 axis, which is also controlled by cAMP/PKA signaling in yeast.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32449834</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1474-9726</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>6</Issue><PubDate><Year>2020</Year><Month>06</Month></PubDate></JournalIssue><Title>Aging cell</Title><ISOAbbreviation>Aging Cell</ISOAbbreviation></Journal><ArticleTitle>TORC1 signaling regulates cytoplasmic pH through Sir2 in yeast.</ArticleTitle><Pagination><MedlinePgn>e13151</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/acel.13151</ELocationID><Abstract><AbstractText>Glucose controls the phosphorylation of silent information regulator 2 (Sir2), a NAD<sup>+</sup> -dependent protein deacetylase, which regulates the expression of the ATP-dependent proton pump Pma1 and replicative lifespan (RLS) in yeast. TORC1 signaling, which is a central regulator of cell growth and lifespan, is regulated by glucose as well as nitrogen sources. In this study, we demonstrate that TORC1 signaling controls Sir2 phosphorylation through casein kinase 2 (CK2) to regulate PMA1 expression and cytoplasmic pH (pHc) in yeast. Inhibition of TORC1 signaling by either TOR1 deletion or rapamycin treatment decreased PMA1 expression, pHc, and vacuolar pH, whereas activation of TORC1 signaling by expressing constitutively active GTR1 (GTR1Q65L) resulted in the opposite phenotypes. Deletion of SIR2 or expression of a phospho-mutant form of SIR2 increased PMA1 expression, pHc, and vacuolar pH in the tor1Δ mutant, suggesting a functional interaction between Sir2 and TORC1 signaling. Furthermore, deletion of TOR1 or KNS1 encoding a LAMMER kinase decreased the phosphorylation level of Sir2, suggesting that TORC1 signaling controls Sir2 phosphorylation. It was also found that Sit4, a protein phosphatase 2A (PP2A)-like phosphatase, and Kns1 are required for TORC1 signaling to regulate PMA1 expression and that TORC1 signaling and the cyclic AMP (cAMP)/protein kinase A (PKA) pathway converge on CK2 to regulate PMA1 expression through Sir2. Taken together, these findings suggest that TORC1 signaling regulates PMA1 expression and pHc through the CK2-Sir2 axis, which is also controlled by cAMP/PKA signaling in yeast.</AbstractText><CopyrightInformation>© 2020 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Devare</LastName><ForeName>Mayur Nimbadas</ForeName><Initials>MN</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Yeong Hyeock</ForeName><Initials>YH</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Joohye</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Woo Kyu</ForeName><Initials>WK</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kwon</LastName><ForeName>Ki-Sun</ForeName><Initials>KS</Initials><AffiliationInfo><Affiliation>Aging Intervention Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jeong-Yoon</ForeName><Initials>JY</Initials><Identifier Source="ORCID">0000-0001-5873-2069</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon, Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Aging Cell</MedlineTA><NlmUniqueID>101130839</NlmUniqueID><ISSNLinking>1474-9718</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Saccharomyces cerevisiae
</Keyword><Keyword MajorTopicYN="Y">Pma1</Keyword><Keyword MajorTopicYN="Y">Sir2</Keyword><Keyword MajorTopicYN="Y">TORC1</Keyword><Keyword MajorTopicYN="Y">aging</Keyword><Keyword MajorTopicYN="Y">cytoplasmic pH</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>01</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>03</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>03</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Hyeock Kim</name><name sortKey="Kwon, Ki Sun" sort="Kwon, Ki Sun" uniqKey="Kwon K" first="Ki-Sun" last="Kwon">Ki-Sun Kwon</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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