Mds3 regulates morphogenesis in Candida albicans through the TOR pathway.
Identifieur interne : 001417 ( Main/Exploration ); précédent : 001416; suivant : 001418Mds3 regulates morphogenesis in Candida albicans through the TOR pathway.
Auteurs : Lucia F. Zacchi [États-Unis] ; Jonatan Gomez-Raja ; Dana A. DavisSource :
- Molecular and cellular biology [ 1098-5549 ] ; 2010.
Descripteurs français
- KwdFr :
- ADN fongique (génétique), Amorces ADN (génétique), Candida albicans (croissance et développement), Candida albicans (génétique), Candida albicans (métabolisme), Candida albicans (pathogénicité), Gènes fongiques (MeSH), Humains (MeSH), Morphogenèse (effets des médicaments et des substances chimiques), Morphogenèse (génétique), Morphogenèse (physiologie), Mutation (MeSH), Protéines fongiques (génétique), Protéines fongiques (métabolisme), Régulation de l'expression des gènes au cours du développement (effets des médicaments et des substances chimiques), Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques), Sirolimus (pharmacologie), Séquence nucléotidique (MeSH), Séquençage par oligonucléotides en batterie (MeSH), Transduction du signal (effets des médicaments et des substances chimiques).
- MESH :
- croissance et développement : Candida albicans.
- effets des médicaments et des substances chimiques : Morphogenèse, Régulation de l'expression des gènes au cours du développement, Régulation de l'expression des gènes fongiques, Transduction du signal.
- génétique : ADN fongique, Amorces ADN, Candida albicans, Morphogenèse, Protéines fongiques.
- métabolisme : Candida albicans, Protéines fongiques.
- pathogénicité : Candida albicans.
- pharmacologie : Sirolimus.
- physiologie : Morphogenèse.
- Gènes fongiques, Humains, Mutation, Séquence nucléotidique, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Base Sequence (MeSH), Candida albicans (genetics), Candida albicans (growth & development), Candida albicans (metabolism), Candida albicans (pathogenicity), DNA Primers (genetics), DNA, Fungal (genetics), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Regulation, Developmental (drug effects), Gene Expression Regulation, Fungal (drug effects), Genes, Fungal (MeSH), Humans (MeSH), Morphogenesis (drug effects), Morphogenesis (genetics), Morphogenesis (physiology), Mutation (MeSH), Oligonucleotide Array Sequence Analysis (MeSH), Signal Transduction (drug effects), Sirolimus (pharmacology).
- MESH :
- chemical , genetics : DNA Primers, DNA, Fungal, Fungal Proteins.
- drug effects : Gene Expression Regulation, Developmental, Gene Expression Regulation, Fungal, Morphogenesis, Signal Transduction.
- genetics : Candida albicans, Morphogenesis.
- growth & development : Candida albicans.
- metabolism : Candida albicans, Fungal Proteins.
- pathogenicity : Candida albicans.
- chemical , pharmacology : Sirolimus.
- physiology : Morphogenesis.
- Base Sequence, Genes, Fungal, Humans, Mutation, Oligonucleotide Array Sequence Analysis.
Abstract
The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3 Delta/Delta cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3 Delta/Delta mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1 Delta/Delta deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4 Delta/Delta and mds3 Delta/Delta mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.
DOI: 10.1128/MCB.01540-09
PubMed: 20457806
PubMed Central: PMC2897559
Affiliations:
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Le document en format XML
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pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3 Delta/Delta cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3 Delta/Delta mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1 Delta/Delta deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4 Delta/Delta and mds3 Delta/Delta mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20457806</PMID><DateCompleted><Year>2010</Year><Month>07</Month><Day>14</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5549</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>14</Issue><PubDate><Year>2010</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Molecular and cellular biology</Title><ISOAbbreviation>Mol Cell Biol</ISOAbbreviation></Journal><ArticleTitle>Mds3 regulates morphogenesis in Candida albicans through the TOR pathway.</ArticleTitle><Pagination><MedlinePgn>3695-710</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/MCB.01540-09</ELocationID><Abstract><AbstractText>The success of Candida albicans as a major human fungal pathogen is dependent on its ability to colonize and survive as a commensal on diverse mucosal surfaces. One trait required for survival and virulence in the host is the morphogenetic yeast-to-hypha transition. Mds3 was identified as a regulator of pH-dependent morphogenesis that functions in parallel with the classic Rim101 pH-sensing pathway. Microarray analyses revealed that mds3 Delta/Delta cells had an expression profile indicative of a hyperactive TOR pathway, including the preferential expression of genes encoding ribosomal proteins and a decreased expression of genes involved in nitrogen source utilization. The transcriptional and morphological defects of the mds3 Delta/Delta mutant were rescued by rapamycin, an inhibitor of TOR, and this rescue was lost in strains carrying the rapamycin-resistant TOR1-1 allele or an rbp1 Delta/Delta deletion. Rapamycin also rescued the transcriptional and morphological defects associated with the loss of Sit4, a TOR pathway effector, but not the loss of Rim101 or Ras1. The sit4 Delta/Delta and mds3 Delta/Delta mutants had additional phenotypic similarities, suggesting that Sit4 and Mds3 function similarly in the TOR pathway. Finally, we found that Mds3 and Sit4 coimmunoprecipitate. Thus, Mds3 is a new member of the TOR pathway that contributes to morphogenesis in C. albicans as a regulator of this key morphogenetic pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zacchi</LastName><ForeName>Lucia F</ForeName><Initials>LF</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 55455, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gomez-Raja</LastName><ForeName>Jonatan</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Davis</LastName><ForeName>Dana A</ForeName><Initials>DA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI064054</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-AI064054</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>05</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell Biol</MedlineTA><NlmUniqueID>8109087</NlmUniqueID><ISSNLinking>0270-7306</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004271">DNA, Fungal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002176" MajorTopicYN="N">Candida albicans</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004271" MajorTopicYN="N">DNA, Fungal</DescriptorName><QualifierName 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MajorTopicYN="N">Morphogenesis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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