Fission Yeast SCYL1/2 Homologue Ppk32: A Novel Regulator of TOR Signalling That Governs Survival during Brefeldin A Induced Stress to Protein Trafficking.
Identifieur interne : 000B05 ( Main/Exploration ); précédent : 000B04; suivant : 000B06Fission Yeast SCYL1/2 Homologue Ppk32: A Novel Regulator of TOR Signalling That Governs Survival during Brefeldin A Induced Stress to Protein Trafficking.
Auteurs : Katarzyna M. Kowalczyk [Royaume-Uni] ; Janni Petersen [Royaume-Uni, Australie]Source :
- PLoS genetics [ 1553-7404 ] ; 2016.
Descripteurs français
- KwdFr :
- Appareil de Golgi (effets des médicaments et des substances chimiques), Appareil de Golgi (génétique), Bréfeldine A (pharmacologie), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexe-2 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (génétique), Lysosomes (effets des médicaments et des substances chimiques), Lysosomes (génétique), Membrane cellulaire (effets des médicaments et des substances chimiques), Membrane cellulaire (génétique), Phosphorylation (MeSH), Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques), Réticulum endoplasmique (effets des médicaments et des substances chimiques), Réticulum endoplasmique (génétique), Schizosaccharomyces (croissance et développement), Schizosaccharomyces (génétique), Sirolimus (métabolisme), Stress physiologique (effets des médicaments et des substances chimiques), Stress physiologique (génétique), Survie cellulaire (effets des médicaments et des substances chimiques), Survie cellulaire (génétique), Sérine-thréonine kinases TOR (génétique), Transport des protéines (effets des médicaments et des substances chimiques), Transport des protéines (génétique), Vacuoles (effets des médicaments et des substances chimiques), Vacuoles (génétique).
- MESH :
- croissance et développement : Schizosaccharomyces.
- effets des médicaments et des substances chimiques : Appareil de Golgi, Lysosomes, Membrane cellulaire, Régulation de l'expression des gènes fongiques, Réticulum endoplasmique, Stress physiologique, Survie cellulaire, Transport des protéines, Vacuoles.
- génétique : Appareil de Golgi, Complexes multiprotéiques, Lysosomes, Membrane cellulaire, Réticulum endoplasmique, Schizosaccharomyces, Stress physiologique, Survie cellulaire, Sérine-thréonine kinases TOR, Transport des protéines, Vacuoles.
- métabolisme : Sirolimus.
- pharmacologie : Bréfeldine A.
- Complexe-1 cible mécanistique de la rapamycine, Complexe-2 cible mécanistique de la rapamycine, Phosphorylation.
English descriptors
- KwdEn :
- Brefeldin A (pharmacology), Cell Membrane (drug effects), Cell Membrane (genetics), Cell Survival (drug effects), Cell Survival (genetics), Endoplasmic Reticulum (drug effects), Endoplasmic Reticulum (genetics), Gene Expression Regulation, Fungal (drug effects), Golgi Apparatus (drug effects), Golgi Apparatus (genetics), Lysosomes (drug effects), Lysosomes (genetics), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mechanistic Target of Rapamycin Complex 2 (MeSH), Multiprotein Complexes (genetics), Phosphorylation (MeSH), Protein Transport (drug effects), Protein Transport (genetics), Schizosaccharomyces (genetics), Schizosaccharomyces (growth & development), Sirolimus (metabolism), Stress, Physiological (drug effects), Stress, Physiological (genetics), TOR Serine-Threonine Kinases (genetics), Vacuoles (drug effects), Vacuoles (genetics).
- MESH :
- chemical , genetics : Multiprotein Complexes, TOR Serine-Threonine Kinases.
- chemical , metabolism : Sirolimus.
- chemical , pharmacology : Brefeldin A.
- drug effects : Cell Membrane, Cell Survival, Endoplasmic Reticulum, Gene Expression Regulation, Fungal, Golgi Apparatus, Lysosomes, Protein Transport, Stress, Physiological, Vacuoles.
- genetics : Cell Membrane, Cell Survival, Endoplasmic Reticulum, Golgi Apparatus, Lysosomes, Protein Transport, Schizosaccharomyces, Stress, Physiological, Vacuoles.
- growth & development : Schizosaccharomyces.
- chemical : Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Phosphorylation.
Abstract
Target of Rapamycin (TOR) signalling allows eukaryotic cells to adjust cell growth in response to changes in their nutritional and environmental context. The two distinct TOR complexes (TORC1/2) localise to the cell's internal membrane compartments; the endoplasmic reticulum (ER), Golgi apparatus and lysosomes/vacuoles. Here, we show that Ppk32, a SCYL family pseudo-kinase, is a novel regulator of TOR signalling. The absence of ppk32 expression confers resistance to TOR inhibition. Ppk32 inhibition of TORC1 is critical for cell survival following Brefeldin A (BFA) induced stress. Treatment of wild type cells with either the TORC1 specific inhibitor rapamycin or the general TOR inhibitor Torin1 confirmed that a reduction in TORC1 activity promoted recovery from BFA induced stress. Phosphorylation of Ppk32 on two residues that are conserved within the SCYL pseudo-kinase family are required for this TOR inhibition. Phosphorylation on these sites controls Ppk32 protein levels and sensitivity to BFA. BFA induced ER stress does not account for the response to BFA that we report here, however BFA is also known to induce Golgi stress and impair traffic to lysosomes. In summary, Ppk32 reduce TOR signalling in response to BFA induced stress to support cell survival.
DOI: 10.1371/journal.pgen.1006041
PubMed: 27191590
PubMed Central: PMC4871519
Affiliations:
Links toward previous steps (curation, corpus...)
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(genetics)</term><term>Schizosaccharomyces (genetics)</term><term>Schizosaccharomyces (growth & development)</term><term>Sirolimus (metabolism)</term><term>Stress, Physiological (drug effects)</term><term>Stress, Physiological (genetics)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>Vacuoles (drug effects)</term><term>Vacuoles (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Appareil de Golgi (effets des médicaments et des substances chimiques)</term><term>Appareil de Golgi (génétique)</term><term>Bréfeldine A (pharmacologie)</term><term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term><term>Complexe-2 cible mécanistique de la rapamycine (MeSH)</term><term>Complexes multiprotéiques (génétique)</term><term>Lysosomes (effets des médicaments et des substances chimiques)</term><term>Lysosomes (génétique)</term><term>Membrane cellulaire (effets des médicaments et des substances chimiques)</term><term>Membrane cellulaire (génétique)</term><term>Phosphorylation (MeSH)</term><term>Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques)</term><term>Réticulum endoplasmique (effets des médicaments et des substances chimiques)</term><term>Réticulum endoplasmique (génétique)</term><term>Schizosaccharomyces (croissance et développement)</term><term>Schizosaccharomyces (génétique)</term><term>Sirolimus (métabolisme)</term><term>Stress physiologique (effets des médicaments et des substances chimiques)</term><term>Stress physiologique (génétique)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Survie cellulaire (génétique)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Transport des protéines (effets des médicaments et des substances chimiques)</term><term>Transport des protéines (génétique)</term><term>Vacuoles (effets des médicaments et des substances chimiques)</term><term>Vacuoles (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Multiprotein Complexes</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Brefeldin A</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Schizosaccharomyces</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Membrane</term><term>Cell Survival</term><term>Endoplasmic Reticulum</term><term>Gene Expression Regulation, Fungal</term><term>Golgi Apparatus</term><term>Lysosomes</term><term>Protein Transport</term><term>Stress, Physiological</term><term>Vacuoles</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Appareil de Golgi</term><term>Lysosomes</term><term>Membrane cellulaire</term><term>Régulation de l'expression des gènes fongiques</term><term>Réticulum endoplasmique</term><term>Stress physiologique</term><term>Survie cellulaire</term><term>Transport des protéines</term><term>Vacuoles</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Membrane</term><term>Cell Survival</term><term>Endoplasmic Reticulum</term><term>Golgi Apparatus</term><term>Lysosomes</term><term>Protein Transport</term><term>Schizosaccharomyces</term><term>Stress, Physiological</term><term>Vacuoles</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Schizosaccharomyces</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Appareil de Golgi</term><term>Complexes multiprotéiques</term><term>Lysosomes</term><term>Membrane cellulaire</term><term>Réticulum endoplasmique</term><term>Schizosaccharomyces</term><term>Stress physiologique</term><term>Survie cellulaire</term><term>Sérine-thréonine kinases TOR</term><term>Transport des protéines</term><term>Vacuoles</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Bréfeldine A</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</term><term>Mechanistic Target of Rapamycin Complex 2</term><term>Phosphorylation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Complexe-2 cible mécanistique de la rapamycine</term><term>Phosphorylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Target of Rapamycin (TOR) signalling allows eukaryotic cells to adjust cell growth in response to changes in their nutritional and environmental context. The two distinct TOR complexes (TORC1/2) localise to the cell's internal membrane compartments; the endoplasmic reticulum (ER), Golgi apparatus and lysosomes/vacuoles. Here, we show that Ppk32, a SCYL family pseudo-kinase, is a novel regulator of TOR signalling. The absence of ppk32 expression confers resistance to TOR inhibition. Ppk32 inhibition of TORC1 is critical for cell survival following Brefeldin A (BFA) induced stress. Treatment of wild type cells with either the TORC1 specific inhibitor rapamycin or the general TOR inhibitor Torin1 confirmed that a reduction in TORC1 activity promoted recovery from BFA induced stress. Phosphorylation of Ppk32 on two residues that are conserved within the SCYL pseudo-kinase family are required for this TOR inhibition. Phosphorylation on these sites controls Ppk32 protein levels and sensitivity to BFA. BFA induced ER stress does not account for the response to BFA that we report here, however BFA is also known to induce Golgi stress and impair traffic to lysosomes. In summary, Ppk32 reduce TOR signalling in response to BFA induced stress to support cell survival.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27191590</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN><JournalIssue CitedMedium="Internet"><Volume>12</Volume><Issue>5</Issue><PubDate><Year>2016</Year><Month>05</Month></PubDate></JournalIssue><Title>PLoS genetics</Title><ISOAbbreviation>PLoS Genet</ISOAbbreviation></Journal><ArticleTitle>Fission Yeast SCYL1/2 Homologue Ppk32: A Novel Regulator of TOR Signalling That Governs Survival during Brefeldin A Induced Stress to Protein Trafficking.</ArticleTitle><Pagination><MedlinePgn>e1006041</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1006041</ELocationID><Abstract><AbstractText>Target of Rapamycin (TOR) signalling allows eukaryotic cells to adjust cell growth in response to changes in their nutritional and environmental context. The two distinct TOR complexes (TORC1/2) localise to the cell's internal membrane compartments; the endoplasmic reticulum (ER), Golgi apparatus and lysosomes/vacuoles. Here, we show that Ppk32, a SCYL family pseudo-kinase, is a novel regulator of TOR signalling. The absence of ppk32 expression confers resistance to TOR inhibition. Ppk32 inhibition of TORC1 is critical for cell survival following Brefeldin A (BFA) induced stress. Treatment of wild type cells with either the TORC1 specific inhibitor rapamycin or the general TOR inhibitor Torin1 confirmed that a reduction in TORC1 activity promoted recovery from BFA induced stress. Phosphorylation of Ppk32 on two residues that are conserved within the SCYL pseudo-kinase family are required for this TOR inhibition. Phosphorylation on these sites controls Ppk32 protein levels and sensitivity to BFA. BFA induced ER stress does not account for the response to BFA that we report here, however BFA is also known to induce Golgi stress and impair traffic to lysosomes. In summary, Ppk32 reduce TOR signalling in response to BFA induced stress to support cell survival.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kowalczyk</LastName><ForeName>Katarzyna M</ForeName><Initials>KM</Initials><Identifier Source="ORCID">0000-0003-2349-7534</Identifier><AffiliationInfo><Affiliation>Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petersen</LastName><ForeName>Janni</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Flinders Centre for Innovation in Cancer, School of Medicine, Flinders University, Adelaide, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>South Australia Health and Medical Research Institute, Adelaide, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>C10888/A9015</GrantID><Agency>Cancer Research UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>C10888/A11178</GrantID><Agency>Cancer Research UK</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Genet</MedlineTA><NlmUniqueID>101239074</NlmUniqueID><ISSNLinking>1553-7390</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046912">Multiprotein Complexes</NameOfSubstance></Chemical><Chemical><RegistryNumber>20350-15-6</RegistryNumber><NameOfSubstance UI="D020126">Brefeldin A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020126" MajorTopicYN="N">Brefeldin A</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002462" MajorTopicYN="N">Cell Membrane</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004721" MajorTopicYN="N">Endoplasmic Reticulum</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006056" MajorTopicYN="N">Golgi Apparatus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046912" MajorTopicYN="N">Multiprotein Complexes</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D021381" MajorTopicYN="N">Protein Transport</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012568" MajorTopicYN="N">Schizosaccharomyces</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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