Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity.
Identifieur interne : 000F94 ( Main/Exploration ); précédent : 000F93; suivant : 000F95Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity.
Auteurs : Chang Su [États-Unis] ; Yang Lu ; Haoping LiuSource :
- Molecular biology of the cell [ 1939-4586 ] ; 2013.
Descripteurs français
- KwdFr :
- Candida albicans (croissance et développement), Candida albicans (cytologie), Candida albicans (enzymologie), Hyphae (croissance et développement), Hyphae (cytologie), Hyphae (enzymologie), Induction enzymatique (MeSH), Liaison aux protéines (MeSH), Mitogen-Activated Protein Kinases (génétique), Mitogen-Activated Protein Kinases (métabolisme), Phénotype (MeSH), Protein Tyrosine Phosphatases (métabolisme), Protéines de répression (métabolisme), Protéines fongiques (métabolisme), Régions promotrices (génétique) (MeSH), Régulation de l'expression des gènes fongiques (MeSH), Régulation positive (MeSH), Sirolimus (pharmacologie), Stress physiologique (MeSH), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
- MESH :
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- croissance et développement : Candida albicans, Hyphae.
- cytologie : Candida albicans, Hyphae.
- enzymologie : Candida albicans, Hyphae.
- génétique : Mitogen-Activated Protein Kinases.
- métabolisme : Mitogen-Activated Protein Kinases, Protein Tyrosine Phosphatases, Protéines de répression, Protéines fongiques, Sérine-thréonine kinases TOR.
- pharmacologie : Sirolimus.
- Induction enzymatique, Liaison aux protéines, Phénotype, Régions promotrices (génétique), Régulation de l'expression des gènes fongiques, Régulation positive, Stress physiologique, Transduction du signal.
English descriptors
- KwdEn :
- Candida albicans (cytology), Candida albicans (enzymology), Candida albicans (growth & development), Enzyme Induction (MeSH), Fungal Proteins (metabolism), Gene Expression Regulation, Fungal (MeSH), Hyphae (cytology), Hyphae (enzymology), Hyphae (growth & development), Mitogen-Activated Protein Kinases (genetics), Mitogen-Activated Protein Kinases (metabolism), Phenotype (MeSH), Promoter Regions, Genetic (MeSH), Protein Binding (MeSH), Protein Tyrosine Phosphatases (metabolism), Repressor Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Stress, Physiological (MeSH), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (metabolism), Up-Regulation (MeSH).
- MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , genetics : Mitogen-Activated Protein Kinases.
- chemical , metabolism : Fungal Proteins, Mitogen-Activated Protein Kinases, Protein Tyrosine Phosphatases, Repressor Proteins, TOR Serine-Threonine Kinases.
- cytology : Candida albicans, Hyphae.
- enzymology : Candida albicans, Hyphae.
- growth & development : Candida albicans, Hyphae.
- chemical , pharmacology : Sirolimus.
- Enzyme Induction, Gene Expression Regulation, Fungal, Phenotype, Promoter Regions, Genetic, Protein Binding, Signal Transduction, Stress, Physiological, Up-Regulation.
Abstract
Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.
DOI: 10.1091/mbc.E12-06-0477
PubMed: 23171549
PubMed Central: PMC3564525
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fungal Proteins</term><term>Mitogen-Activated Protein Kinases</term><term>Protein Tyrosine Phosphatases</term><term>Repressor Proteins</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Candida albicans</term><term>Hyphae</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Candida albicans</term><term>Hyphae</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Candida albicans</term><term>Hyphae</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Candida 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Fungal</term><term>Phenotype</term><term>Promoter Regions, Genetic</term><term>Protein Binding</term><term>Signal Transduction</term><term>Stress, Physiological</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Induction enzymatique</term><term>Liaison aux protéines</term><term>Phénotype</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes fongiques</term><term>Régulation positive</term><term>Stress physiologique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23171549</PMID><DateCompleted><Year>2013</Year><Month>07</Month><Day>23</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1939-4586</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Molecular biology of the cell</Title><ISOAbbreviation>Mol Biol Cell</ISOAbbreviation></Journal><ArticleTitle>Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity.</ArticleTitle><Pagination><MedlinePgn>385-97</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1091/mbc.E12-06-0477</ELocationID><Abstract><AbstractText>Candida albicans is able to undergo reversible morphological changes between yeast and hyphal forms in response to environmental cues. This morphological plasticity is essential for its pathogenesis. Hyphal development requires two temporally linked changes in promoter chromatin, which is sequentially regulated by temporarily clearing the transcription inhibitor Nrg1 upon activation of cAMP/protein kinase A and promoter recruitment of the histone deacetylase Hda1 under reduced target of rapamycin (Tor1) signaling. The GATA family transcription factor Brg1 recruits Hda1 to promoters for sustained hyphal development, and BRG1 expression is a readout of reduced Tor1 signaling. How Tor1 regulates BRG1 expression is not clear. Using a forward genetic screen for mutants that can sustain hyphal elongation in rich media, we found hog1, ssk2, and pbs2 mutants of the HOG mitogen-activated protein kinase pathway to express BRG1 irrespective of rapamycin. Furthermore, rapamycin lowers the basal activity of Hog1 through the functions of the two Hog1 tyrosine phosphatases Ptp2 and Ptp3. Active Hog1 represses the expression of BRG1 via the transcriptional repressor Sko1 as Sko1 disassociates from the promoter of BRG1 in the hog1 mutant or in rapamycin. Our data suggest that reduced Tor1 signaling lowers Hog1 basal activity via Hog1 phosphatases to activate BRG1 expression for hyphal elongation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Chang</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Biological Chemistry, University of California, Irvine, Irvine, CA 92697, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Yang</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Haoping</ForeName><Initials>H</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI099190</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 GM055155</GrantID><Acronym>GM</Acronym><Agency>NIGMS 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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Biol Cell</MedlineTA><NlmUniqueID>9201390</NlmUniqueID><ISSNLinking>1059-1524</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012097">Repressor Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.48</RegistryNumber><NameOfSubstance UI="D017027">Protein Tyrosine Phosphatases</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002176" MajorTopicYN="N">Candida albicans</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004790" MajorTopicYN="N">Enzyme Induction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D025301" MajorTopicYN="N">Hyphae</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020928" MajorTopicYN="N">Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017027" MajorTopicYN="N">Protein Tyrosine Phosphatases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012097" MajorTopicYN="N">Repressor Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>11</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>11</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>7</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23171549</ArticleId><ArticleId IdType="pii">mbc.E12-06-0477</ArticleId><ArticleId IdType="doi">10.1091/mbc.E12-06-0477</ArticleId><ArticleId 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IdType="pubmed">16164545</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><noCountry><name sortKey="Liu, Haoping" sort="Liu, Haoping" uniqKey="Liu H" first="Haoping" last="Liu">Haoping Liu</name><name sortKey="Lu, Yang" sort="Lu, Yang" uniqKey="Lu Y" first="Yang" last="Lu">Yang Lu</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Su, Chang" sort="Su, Chang" uniqKey="Su C" first="Chang" last="Su">Chang Su</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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