The small GTPase Rhb1 is involved in the cell response to fluconazole in Candida albicans.
Identifieur interne : 000190 ( Main/Exploration ); précédent : 000189; suivant : 000191The small GTPase Rhb1 is involved in the cell response to fluconazole in Candida albicans.
Auteurs : Yu-Wen Chen [Taïwan] ; Ying-Chieh Yeh [Taïwan] ; Hsueh-Fen Chen [Taïwan] ; Ruei-Ching Chen [Taïwan] ; Guan-Yu Lin [Taïwan] ; Yu-Ting Chen [Taïwan] ; Chung-Yu Lan [Taïwan]Source :
- FEMS yeast research [ 1567-1364 ] ; 2019.
Descripteurs français
- KwdFr :
- Antifongiques (pharmacologie), Candida albicans (effets des médicaments et des substances chimiques), Candida albicans (génétique), Délétion de gène (MeSH), Fluconazole (pharmacologie), Protéines G monomériques (déficit), Protéines G monomériques (métabolisme), Protéines de transport membranaire (métabolisme), Régulation de l'expression des gènes fongiques (MeSH), Résistance des champignons aux médicaments (MeSH), Tests de sensibilité microbienne (MeSH), Transport biologique actif (MeSH).
- MESH :
- déficit : Protéines G monomériques.
- effets des médicaments et des substances chimiques : Candida albicans.
- génétique : Candida albicans.
- métabolisme : Protéines G monomériques, Protéines de transport membranaire.
- pharmacologie : Antifongiques, Fluconazole.
- Délétion de gène, Régulation de l'expression des gènes fongiques, Résistance des champignons aux médicaments, Tests de sensibilité microbienne, Transport biologique actif.
English descriptors
- KwdEn :
- Antifungal Agents (pharmacology), Biological Transport, Active (MeSH), Candida albicans (drug effects), Candida albicans (genetics), Drug Resistance, Fungal (MeSH), Fluconazole (pharmacology), Gene Deletion (MeSH), Gene Expression Regulation, Fungal (MeSH), Membrane Transport Proteins (metabolism), Microbial Sensitivity Tests (MeSH), Monomeric GTP-Binding Proteins (deficiency), Monomeric GTP-Binding Proteins (metabolism).
- MESH :
- chemical , deficiency : Monomeric GTP-Binding Proteins.
- chemical , metabolism : Membrane Transport Proteins, Monomeric GTP-Binding Proteins.
- chemical , pharmacology : Antifungal Agents, Fluconazole.
- drug effects : Candida albicans.
- genetics : Candida albicans.
- Biological Transport, Active, Drug Resistance, Fungal, Gene Deletion, Gene Expression Regulation, Fungal, Microbial Sensitivity Tests.
Abstract
Candida albicans is an important fungal pathogen in humans. Rhb1 is a small GTPase of the Ras superfamily and is conserved from yeasts to humans. In C. albicans, Rhb1 regulates the expression of secreted protease 2, low nitrogen-mediated morphogenesis, and biofilm formation. Moreover, our previous studies have indicated that Rhb1 is associated with the target of rapamycin (TOR) signaling pathway. In this study, we further explored the relationship between Rhb1 and drug susceptibility. The RHB1 deletion mutant exhibited reduced fluconazole susceptibility, and this phenotype occurred mainly through the increased gene expression and activity of efflux pumps. In addition, Mrr1 and Tac1 are transcription factors that can activate efflux pump gene expression. However, the RHB1 deletion, RHB1/MRR1 and RHB1/TAC1 double deletion mutants had no significant differences in efflux pump gene expression and fluconazole susceptibility, suggesting that Rhb1-regulated efflux pump genes do not act through Mrr1 and Tac1. We also showed that membrane localization is crucial for Rhb1 activity in response to fluconazole. Finally, Rhb1 was linked not only to the TOR but also to the Mkc1 mitogen-activated protein kinase signaling pathway in response to fluconazole. In sum, this study unveiled a new role of Rhb1 in the regulation of C. albicans drug susceptibility.
DOI: 10.1093/femsyr/foz005
PubMed: 30649293
Affiliations:
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uniqKey="Chen Y" first="Yu-Wen" last="Chen">Yu-Wen Chen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Yeh, Ying Chieh" sort="Yeh, Ying Chieh" uniqKey="Yeh Y" first="Ying-Chieh" last="Yeh">Ying-Chieh Yeh</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Hsueh Fen" sort="Chen, Hsueh Fen" uniqKey="Chen H" first="Hsueh-Fen" last="Chen">Hsueh-Fen Chen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Ruei Ching" sort="Chen, Ruei Ching" uniqKey="Chen R" first="Ruei-Ching" last="Chen">Ruei-Ching Chen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Guan Yu" sort="Lin, Guan Yu" uniqKey="Lin G" first="Guan-Yu" last="Lin">Guan-Yu Lin</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Yu Ting" sort="Chen, Yu Ting" uniqKey="Chen Y" first="Yu-Ting" last="Chen">Yu-Ting Chen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author><author><name sortKey="Lan, Chung Yu" sort="Lan, Chung Yu" uniqKey="Lan C" first="Chung-Yu" last="Lan">Chung-Yu Lan</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Life Science, National Tsing Hua University, Hsinchu 30013, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Life Science, National Tsing Hua University, Hsinchu 30013</wicri:regionArea><wicri:noRegion>Hsinchu 30013</wicri:noRegion></affiliation></author></analytic><series><title level="j">FEMS yeast research</title><idno type="eISSN">1567-1364</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antifungal Agents (pharmacology)</term><term>Biological Transport, Active (MeSH)</term><term>Candida albicans (drug effects)</term><term>Candida albicans (genetics)</term><term>Drug Resistance, Fungal (MeSH)</term><term>Fluconazole (pharmacology)</term><term>Gene Deletion (MeSH)</term><term>Gene Expression Regulation, Fungal (MeSH)</term><term>Membrane Transport Proteins (metabolism)</term><term>Microbial Sensitivity Tests (MeSH)</term><term>Monomeric GTP-Binding Proteins (deficiency)</term><term>Monomeric GTP-Binding Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antifongiques (pharmacologie)</term><term>Candida albicans (effets des médicaments et des substances chimiques)</term><term>Candida albicans (génétique)</term><term>Délétion de gène (MeSH)</term><term>Fluconazole (pharmacologie)</term><term>Protéines G monomériques (déficit)</term><term>Protéines G monomériques (métabolisme)</term><term>Protéines de transport membranaire (métabolisme)</term><term>Régulation de l'expression des gènes fongiques (MeSH)</term><term>Résistance des champignons aux médicaments (MeSH)</term><term>Tests de sensibilité microbienne (MeSH)</term><term>Transport biologique actif (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Monomeric GTP-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Membrane Transport Proteins</term><term>Monomeric GTP-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antifungal Agents</term><term>Fluconazole</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Candida albicans</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Protéines G monomériques</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Candida albicans</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Candida albicans</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Candida albicans</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines G monomériques</term><term>Protéines de transport membranaire</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antifongiques</term><term>Fluconazole</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Transport, Active</term><term>Drug Resistance, Fungal</term><term>Gene Deletion</term><term>Gene Expression Regulation, Fungal</term><term>Microbial Sensitivity Tests</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Délétion de gène</term><term>Régulation de l'expression des gènes fongiques</term><term>Résistance des champignons aux médicaments</term><term>Tests de sensibilité microbienne</term><term>Transport biologique actif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Candida albicans is an important fungal pathogen in humans. Rhb1 is a small GTPase of the Ras superfamily and is conserved from yeasts to humans. In C. albicans, Rhb1 regulates the expression of secreted protease 2, low nitrogen-mediated morphogenesis, and biofilm formation. Moreover, our previous studies have indicated that Rhb1 is associated with the target of rapamycin (TOR) signaling pathway. In this study, we further explored the relationship between Rhb1 and drug susceptibility. The RHB1 deletion mutant exhibited reduced fluconazole susceptibility, and this phenotype occurred mainly through the increased gene expression and activity of efflux pumps. In addition, Mrr1 and Tac1 are transcription factors that can activate efflux pump gene expression. However, the RHB1 deletion, RHB1/MRR1 and RHB1/TAC1 double deletion mutants had no significant differences in efflux pump gene expression and fluconazole susceptibility, suggesting that Rhb1-regulated efflux pump genes do not act through Mrr1 and Tac1. We also showed that membrane localization is crucial for Rhb1 activity in response to fluconazole. Finally, Rhb1 was linked not only to the TOR but also to the Mkc1 mitogen-activated protein kinase signaling pathway in response to fluconazole. In sum, this study unveiled a new role of Rhb1 in the regulation of C. albicans drug susceptibility.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30649293</PMID><DateCompleted><Year>2019</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>27</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1567-1364</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>2</Issue><PubDate><Year>2019</Year><Month>03</Month><Day>01</Day></PubDate></JournalIssue><Title>FEMS yeast research</Title><ISOAbbreviation>FEMS Yeast Res</ISOAbbreviation></Journal><ArticleTitle>The small GTPase Rhb1 is involved in the cell response to fluconazole in Candida albicans.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1093/femsyr/foz005</ELocationID><Abstract><AbstractText>Candida albicans is an important fungal pathogen in humans. Rhb1 is a small GTPase of the Ras superfamily and is conserved from yeasts to humans. In C. albicans, Rhb1 regulates the expression of secreted protease 2, low nitrogen-mediated morphogenesis, and biofilm formation. Moreover, our previous studies have indicated that Rhb1 is associated with the target of rapamycin (TOR) signaling pathway. In this study, we further explored the relationship between Rhb1 and drug susceptibility. The RHB1 deletion mutant exhibited reduced fluconazole susceptibility, and this phenotype occurred mainly through the increased gene expression and activity of efflux pumps. In addition, Mrr1 and Tac1 are transcription factors that can activate efflux pump gene expression. However, the RHB1 deletion, RHB1/MRR1 and RHB1/TAC1 double deletion mutants had no significant differences in efflux pump gene expression and fluconazole susceptibility, suggesting that Rhb1-regulated efflux pump genes do not act through Mrr1 and Tac1. We also showed that membrane localization is crucial for Rhb1 activity in response to fluconazole. Finally, Rhb1 was linked not only to the TOR but also to the Mkc1 mitogen-activated protein kinase signaling pathway in response to fluconazole. In sum, this study unveiled a new role of Rhb1 in the regulation of C. albicans drug susceptibility.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yu-Wen</ForeName><Initials>YW</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yeh</LastName><ForeName>Ying-Chieh</ForeName><Initials>YC</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hsueh-Fen</ForeName><Initials>HF</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Ruei-Ching</ForeName><Initials>RC</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Guan-Yu</ForeName><Initials>GY</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yu-Ting</ForeName><Initials>YT</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lan</LastName><ForeName>Chung-Yu</ForeName><Initials>CY</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Cellular Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Life Science, National Tsing Hua University, Hsinchu 30013, Taiwan.</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></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEMS Yeast Res</MedlineTA><NlmUniqueID>101085384</NlmUniqueID><ISSNLinking>1567-1356</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000935">Antifungal Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>8VZV102JFY</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">Fluconazole</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="Y">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="N">Membrane Transport Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008826" MajorTopicYN="N">Microbial Sensitivity Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020559" MajorTopicYN="N">Monomeric GTP-Binding Proteins</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>03</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>01</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>1</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>8</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>1</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30649293</ArticleId><ArticleId IdType="pii">5288341</ArticleId><ArticleId IdType="doi">10.1093/femsyr/foz005</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Chen, Yu Wen" sort="Chen, Yu Wen" uniqKey="Chen Y" first="Yu-Wen" last="Chen">Yu-Wen Chen</name></noRegion><name sortKey="Chen, Hsueh Fen" sort="Chen, Hsueh Fen" uniqKey="Chen H" first="Hsueh-Fen" last="Chen">Hsueh-Fen Chen</name><name sortKey="Chen, Ruei Ching" sort="Chen, Ruei Ching" uniqKey="Chen R" first="Ruei-Ching" last="Chen">Ruei-Ching Chen</name><name sortKey="Chen, Yu Ting" sort="Chen, Yu Ting" uniqKey="Chen Y" first="Yu-Ting" last="Chen">Yu-Ting Chen</name><name sortKey="Lan, Chung Yu" sort="Lan, Chung Yu" uniqKey="Lan C" first="Chung-Yu" last="Lan">Chung-Yu Lan</name><name sortKey="Lan, Chung Yu" sort="Lan, Chung Yu" uniqKey="Lan C" first="Chung-Yu" last="Lan">Chung-Yu Lan</name><name sortKey="Lin, Guan Yu" sort="Lin, Guan Yu" uniqKey="Lin G" first="Guan-Yu" last="Lin">Guan-Yu Lin</name><name sortKey="Yeh, Ying Chieh" sort="Yeh, Ying Chieh" uniqKey="Yeh Y" first="Ying-Chieh" last="Yeh">Ying-Chieh Yeh</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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