Group A Streptococcus modulates RAB1- and PIK3C3 complex-dependent autophagy.
Identifieur interne : 000115 ( Main/Exploration ); précédent : 000114; suivant : 000116Group A Streptococcus modulates RAB1- and PIK3C3 complex-dependent autophagy.
Auteurs : Hirotaka Toh [Japon] ; Takashi Nozawa [Japon] ; Atsuko Minowa-Nozawa [Japon] ; Miyako Hikichi [Japon] ; Shintaro Nakajima [Japon] ; Chihiro Aikawa [Japon] ; Ichiro Nakagawa [Japon]Source :
- Autophagy [ 1554-8635 ] ; 2020.
Abstract
Autophagy selectively targets invading bacteria to defend cells, whereas bacterial pathogens counteract autophagy to survive in cells. The initiation of canonical autophagy involves the PIK3C3 complex, but autophagy targeting Group A Streptococcus (GAS) is PIK3C3-independent. We report that GAS infection elicits both PIK3C3-dependent and -independent autophagy, and that the GAS effector NAD-glycohydrolase (Nga) selectively modulates PIK3C3-dependent autophagy. GAS regulates starvation-induced (canonical) PIK3C3-dependent autophagy by secreting streptolysin O and Nga, and Nga also suppresses PIK3C3-dependent GAS-targeting-autophagosome formation during early infection and facilitates intracellular proliferation. This Nga-sensitive autophagosome formation involves the ATG14-containing PIK3C3 complex and RAB1 GTPase, which are both dispensable for Nga-insensitive RAB9A/RAB17-positive autophagosome formation. Furthermore, although MTOR inhibition and subsequent activation of ULK1, BECN1, and ATG14 occur during GAS infection, ATG14 recruitment to GAS is impaired, suggesting that Nga inhibits the recruitment of ATG14-containing PIK3C3 complexes to autophagosome-formation sites. Our findings reveal not only a previously unrecognized GAS-host interaction that modulates canonical autophagy, but also the existence of multiple autophagy pathways, using distinct regulators, targeting bacterial infection.Abbreviations: ATG5: autophagy related 5; ATG14: autophagy related 14; ATG16L1: autophagy related 16 like 1; BECN1: beclin 1; CALCOCO2: calcium binding and coiled-coil domain 2; GAS: group A streptococcus; GcAV: GAS-containing autophagosome-like vacuole; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTORC1: mechanistic target of rapamycin kinase complex 1; Nga: NAD-glycohydrolase; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4P: phosphatidylinositol-4-phosphate; RAB: RAB, member RAS oncogene GTPases; RAB1A: RAB1A, member RAS oncogene family; RAB11A: RAB11A, member RAS oncogene family; RAB17: RAB17, member RAS oncogene family; RAB24: RAB24, member RAS oncogene family; RPS6KB1: ribosomal protein S6 kinase B1; SLO: streptolysin O; SQSTM1: sequestosome 1; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2.
DOI: 10.1080/15548627.2019.1628539
PubMed: 31177902
PubMed Central: PMC6984453
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first="Hirotaka" last="Toh">Hirotaka Toh</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Nozawa, Takashi" sort="Nozawa, Takashi" uniqKey="Nozawa T" first="Takashi" last="Nozawa">Takashi Nozawa</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Minowa Nozawa, Atsuko" sort="Minowa Nozawa, Atsuko" uniqKey="Minowa Nozawa A" first="Atsuko" last="Minowa-Nozawa">Atsuko Minowa-Nozawa</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Hikichi, Miyako" sort="Hikichi, Miyako" uniqKey="Hikichi M" first="Miyako" last="Hikichi">Miyako Hikichi</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Nakajima, Shintaro" sort="Nakajima, Shintaro" uniqKey="Nakajima S" first="Shintaro" last="Nakajima">Shintaro Nakajima</name><affiliation wicri:level="3"><nlm:affiliation>Department of Life Science Dentistry, The Nippon Dental University, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Life Science Dentistry, The Nippon Dental University, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>Department of Developmental and Regenerative Dentistry, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Developmental and Regenerative Dentistry, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Aikawa, Chihiro" sort="Aikawa, Chihiro" uniqKey="Aikawa C" first="Chihiro" last="Aikawa">Chihiro Aikawa</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Nakagawa, Ichiro" sort="Nakagawa, Ichiro" uniqKey="Nakagawa I" first="Ichiro" last="Nakagawa">Ichiro Nakagawa</name><affiliation wicri:level="4"><nlm:affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</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">Autophagy selectively targets invading bacteria to defend cells, whereas bacterial pathogens counteract autophagy to survive in cells. The initiation of canonical autophagy involves the PIK3C3 complex, but autophagy targeting Group A <i>Streptococcus</i> (GAS) is PIK3C3-independent. We report that GAS infection elicits both PIK3C3-dependent and -independent autophagy, and that the GAS effector NAD-glycohydrolase (Nga) selectively modulates PIK3C3-dependent autophagy. GAS regulates starvation-induced (canonical) PIK3C3-dependent autophagy by secreting streptolysin O and Nga, and Nga also suppresses PIK3C3-dependent GAS-targeting-autophagosome formation during early infection and facilitates intracellular proliferation. This Nga-sensitive autophagosome formation involves the ATG14-containing PIK3C3 complex and RAB1 GTPase, which are both dispensable for Nga-insensitive RAB9A/RAB17-positive autophagosome formation. Furthermore, although MTOR inhibition and subsequent activation of ULK1, BECN1, and ATG14 occur during GAS infection, ATG14 recruitment to GAS is impaired, suggesting that Nga inhibits the recruitment of ATG14-containing PIK3C3 complexes to autophagosome-formation sites. Our findings reveal not only a previously unrecognized GAS-host interaction that modulates canonical autophagy, but also the existence of multiple autophagy pathways, using distinct regulators, targeting bacterial infection.<b>Abbreviations</b>: ATG5: autophagy related 5; ATG14: autophagy related 14; ATG16L1: autophagy related 16 like 1; BECN1: beclin 1; CALCOCO2: calcium binding and coiled-coil domain 2; GAS: group A <i>streptococcus</i>; GcAV: GAS-containing autophagosome-like vacuole; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTORC1: mechanistic target of rapamycin kinase complex 1; Nga: NAD-glycohydrolase; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4P: phosphatidylinositol-4-phosphate; RAB: RAB, member RAS oncogene GTPases; RAB1A: RAB1A, member RAS oncogene family; RAB11A: RAB11A, member RAS oncogene family; RAB17: RAB17, member RAS oncogene family; RAB24: RAB24, member RAS oncogene family; RPS6KB1: ribosomal protein S6 kinase B1; SLO: streptolysin O; SQSTM1: sequestosome 1; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">31177902</PMID><DateRevised><Year>2020</Year><Month>06</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>02</Month></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>Group A <i>Streptococcus</i> modulates RAB1- and PIK3C3 complex-dependent autophagy.</ArticleTitle><Pagination><MedlinePgn>334-346</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2019.1628539</ELocationID><Abstract><AbstractText>Autophagy selectively targets invading bacteria to defend cells, whereas bacterial pathogens counteract autophagy to survive in cells. The initiation of canonical autophagy involves the PIK3C3 complex, but autophagy targeting Group A <i>Streptococcus</i> (GAS) is PIK3C3-independent. We report that GAS infection elicits both PIK3C3-dependent and -independent autophagy, and that the GAS effector NAD-glycohydrolase (Nga) selectively modulates PIK3C3-dependent autophagy. GAS regulates starvation-induced (canonical) PIK3C3-dependent autophagy by secreting streptolysin O and Nga, and Nga also suppresses PIK3C3-dependent GAS-targeting-autophagosome formation during early infection and facilitates intracellular proliferation. This Nga-sensitive autophagosome formation involves the ATG14-containing PIK3C3 complex and RAB1 GTPase, which are both dispensable for Nga-insensitive RAB9A/RAB17-positive autophagosome formation. Furthermore, although MTOR inhibition and subsequent activation of ULK1, BECN1, and ATG14 occur during GAS infection, ATG14 recruitment to GAS is impaired, suggesting that Nga inhibits the recruitment of ATG14-containing PIK3C3 complexes to autophagosome-formation sites. Our findings reveal not only a previously unrecognized GAS-host interaction that modulates canonical autophagy, but also the existence of multiple autophagy pathways, using distinct regulators, targeting bacterial infection.<b>Abbreviations</b>: ATG5: autophagy related 5; ATG14: autophagy related 14; ATG16L1: autophagy related 16 like 1; BECN1: beclin 1; CALCOCO2: calcium binding and coiled-coil domain 2; GAS: group A <i>streptococcus</i>; GcAV: GAS-containing autophagosome-like vacuole; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTORC1: mechanistic target of rapamycin kinase complex 1; Nga: NAD-glycohydrolase; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PtdIns3P: phosphatidylinositol-3-phosphate; PtdIns4P: phosphatidylinositol-4-phosphate; RAB: RAB, member RAS oncogene GTPases; RAB1A: RAB1A, member RAS oncogene family; RAB11A: RAB11A, member RAS oncogene family; RAB17: RAB17, member RAS oncogene family; RAB24: RAB24, member RAS oncogene family; RPS6KB1: ribosomal protein S6 kinase B1; SLO: streptolysin O; SQSTM1: sequestosome 1; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Toh</LastName><ForeName>Hirotaka</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nozawa</LastName><ForeName>Takashi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Minowa-Nozawa</LastName><ForeName>Atsuko</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hikichi</LastName><ForeName>Miyako</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakajima</LastName><ForeName>Shintaro</ForeName><Initials>S</Initials><Identifier Source="ORCID">0000-0003-4858-3391</Identifier><AffiliationInfo><Affiliation>Department of Life Science Dentistry, The Nippon Dental University, Tokyo, Japan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Developmental and Regenerative Dentistry, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aikawa</LastName><ForeName>Chihiro</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nakagawa</LastName><ForeName>Ichiro</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0001-6552-1702</Identifier><AffiliationInfo><Affiliation>Department of Microbiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.</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>2019</Year><Month>06</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Autophagy</MedlineTA><NlmUniqueID>101265188</NlmUniqueID><ISSNLinking>1554-8627</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">NAD-glycohydrolase</Keyword><Keyword MajorTopicYN="Y">PIK3C3</Keyword><Keyword MajorTopicYN="Y">RAB GTPase</Keyword><Keyword MajorTopicYN="Y">group A Streptococcus</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31177902</ArticleId><ArticleId IdType="doi">10.1080/15548627.2019.1628539</ArticleId><ArticleId IdType="pmc">PMC6984453</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Autophagy. 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Kansai"><name sortKey="Toh, Hirotaka" sort="Toh, Hirotaka" uniqKey="Toh H" first="Hirotaka" last="Toh">Hirotaka Toh</name></region><name sortKey="Aikawa, Chihiro" sort="Aikawa, Chihiro" uniqKey="Aikawa C" first="Chihiro" last="Aikawa">Chihiro Aikawa</name><name sortKey="Hikichi, Miyako" sort="Hikichi, Miyako" uniqKey="Hikichi M" first="Miyako" last="Hikichi">Miyako Hikichi</name><name sortKey="Minowa Nozawa, Atsuko" sort="Minowa Nozawa, Atsuko" uniqKey="Minowa Nozawa A" first="Atsuko" last="Minowa-Nozawa">Atsuko Minowa-Nozawa</name><name sortKey="Nakagawa, Ichiro" sort="Nakagawa, Ichiro" uniqKey="Nakagawa I" first="Ichiro" last="Nakagawa">Ichiro Nakagawa</name><name sortKey="Nakajima, Shintaro" sort="Nakajima, Shintaro" uniqKey="Nakajima S" first="Shintaro" last="Nakajima">Shintaro Nakajima</name><name sortKey="Nakajima, Shintaro" sort="Nakajima, Shintaro" uniqKey="Nakajima S" first="Shintaro" last="Nakajima">Shintaro Nakajima</name><name sortKey="Nozawa, Takashi" sort="Nozawa, Takashi" uniqKey="Nozawa T" first="Takashi" last="Nozawa">Takashi Nozawa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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