The Candida albicans TOR-Activating GTPases Gtr1 and Rhb1 Coregulate Starvation Responses and Biofilm Formation.
Identifieur interne : 000680 ( Main/Exploration ); précédent : 000679; suivant : 000681The Candida albicans TOR-Activating GTPases Gtr1 and Rhb1 Coregulate Starvation Responses and Biofilm Formation.
Auteurs : Peter R. Flanagan [Irlande (pays)] ; Ning-Ning Liu [États-Unis] ; Darren J. Fitzpatrick [Irlande (pays)] ; Karsten Hokamp [Irlande (pays)] ; Julia R. Köhler [États-Unis] ; Gary P. Moran [Irlande (pays)]Source :
- mSphere [ 2379-5042 ]
Abstract
Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in eukaryotic cells and in the fungal pathogen Candida albicans regulates morphogenesis and nitrogen acquisition. Gtr1 encodes a highly conserved GTPase that in Saccharomyces cerevisiae regulates nitrogen sensing and TORC1 activation. Here, we characterize the role of C. albicans GTR1 in TORC1 activation and compare it with the previously characterized GTPase Rhb1. A homozygous gtr1/gtr1 mutant exhibited impaired TORC1-mediated phosphorylation of ribosomal protein S6 and increased susceptibility to rapamycin. Overexpression of GTR1 impaired nitrogen starvation-induced filamentous growth, MEP2 expression, and growth in bovine serum albumin as the sole nitrogen source. Both GTR1 and RHB1 were shown to regulate genes involved in ribosome biogenesis, amino acid biosynthesis, and expression of biofilm growth-induced genes. The rhb1/rhb1 mutant exhibited a different pattern of expression of Sko1-regulated genes and increased susceptibility to Congo red and calcofluor white. The homozygous gtr1/gtr1 mutant exhibited enhanced flocculation phenotypes and, similar to the rhb1/rhb1 mutant, exhibited enhanced biofilm formation on plastic surfaces. In summary, Gtr1 and Rhb1 link nutrient sensing and biofilm formation and this connectivity may have evolved to enhance the competitiveness of C. albicans in niches where there is intense competition with other microbes for space and nutrients. IMPORTANCECandida albicans is the major fungal pathogen of humans and is responsible for a wide range of infections, including life-threatening systemic infections in susceptible hosts. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in this fungus, and components of this complex are under increased investigation as targets for new antifungal drugs. The present study characterized the role of GTR1, encoding a putative GTPase, in TORC1 activation. This study shows that GTR1 encodes a protein required for activation of TORC1 activity in response to amino acids and regulation of nitrogen starvation responses. GTR1 mutants show increased cell-cell adhesion and biofilm formation and increased expression of genes involved in these processes. This study demonstrates that starvation responses and biofilm formation are coregulated by GTR1 and suggests that these responses are linked to compete with the microbiome for space and nutrients.
DOI: 10.1128/mSphere.00477-17
PubMed: 29152581
PubMed Central: PMC5687921
Affiliations:
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Flanagan</name><affiliation wicri:level="1"><nlm:affiliation>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin, Ireland.</nlm:affiliation><country xml:lang="fr">Irlande (pays)</country><wicri:regionArea>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin</wicri:regionArea><wicri:noRegion>Dublin</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Ning Ning" sort="Liu, Ning Ning" uniqKey="Liu N" first="Ning-Ning" last="Liu">Ning-Ning Liu</name><affiliation wicri:level="2"><nlm:affiliation>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Fitzpatrick, Darren J" sort="Fitzpatrick, Darren J" uniqKey="Fitzpatrick D" first="Darren J" last="Fitzpatrick">Darren J. Fitzpatrick</name><affiliation wicri:level="1"><nlm:affiliation>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin, Ireland.</nlm:affiliation><country xml:lang="fr">Irlande (pays)</country><wicri:regionArea>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin</wicri:regionArea><wicri:noRegion>Dublin</wicri:noRegion></affiliation></author><author><name sortKey="Hokamp, Karsten" sort="Hokamp, Karsten" uniqKey="Hokamp K" first="Karsten" last="Hokamp">Karsten Hokamp</name><affiliation wicri:level="1"><nlm:affiliation>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin, Ireland.</nlm:affiliation><country xml:lang="fr">Irlande (pays)</country><wicri:regionArea>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin</wicri:regionArea><wicri:noRegion>Dublin</wicri:noRegion></affiliation></author><author><name sortKey="Kohler, Julia R" sort="Kohler, Julia R" uniqKey="Kohler J" first="Julia R" last="Köhler">Julia R. Köhler</name><affiliation wicri:level="2"><nlm:affiliation>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Moran, Gary P" sort="Moran, Gary P" uniqKey="Moran G" first="Gary P" last="Moran">Gary P. Moran</name><affiliation wicri:level="1"><nlm:affiliation>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin, Ireland.</nlm:affiliation><country xml:lang="fr">Irlande (pays)</country><wicri:regionArea>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin</wicri:regionArea><wicri:noRegion>Dublin</wicri:noRegion></affiliation></author></analytic><series><title level="j">mSphere</title><idno type="ISSN">2379-5042</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in eukaryotic cells and in the fungal pathogen <i>Candida albicans</i> regulates morphogenesis and nitrogen acquisition. Gtr1 encodes a highly conserved GTPase that in <i>Saccharomyces cerevisiae</i> regulates nitrogen sensing and TORC1 activation. Here, we characterize the role of <i>C. albicans GTR1</i> in TORC1 activation and compare it with the previously characterized GTPase Rhb1. A homozygous <i>gtr1/gtr1</i> mutant exhibited impaired TORC1-mediated phosphorylation of ribosomal protein S6 and increased susceptibility to rapamycin. Overexpression of <i>GTR1</i> impaired nitrogen starvation-induced filamentous growth, <i>MEP2</i> expression, and growth in bovine serum albumin as the sole nitrogen source. Both <i>GTR1</i> and <i>RHB1</i> were shown to regulate genes involved in ribosome biogenesis, amino acid biosynthesis, and expression of biofilm growth-induced genes. The <i>rhb1/rhb1</i> mutant exhibited a different pattern of expression of Sko1-regulated genes and increased susceptibility to Congo red and calcofluor white. The homozygous <i>gtr1/gtr1</i> mutant exhibited enhanced flocculation phenotypes and, similar to the <i>rhb1/rhb1</i> mutant, exhibited enhanced biofilm formation on plastic surfaces. In summary, Gtr1 and Rhb1 link nutrient sensing and biofilm formation and this connectivity may have evolved to enhance the competitiveness of <i>C. albicans</i> in niches where there is intense competition with other microbes for space and nutrients. <b>IMPORTANCE</b><i>Candida albicans</i> is the major fungal pathogen of humans and is responsible for a wide range of infections, including life-threatening systemic infections in susceptible hosts. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in this fungus, and components of this complex are under increased investigation as targets for new antifungal drugs. The present study characterized the role of <i>GTR1</i>, encoding a putative GTPase, in TORC1 activation. This study shows that <i>GTR1</i> encodes a protein required for activation of TORC1 activity in response to amino acids and regulation of nitrogen starvation responses. <i>GTR1</i> mutants show increased cell-cell adhesion and biofilm formation and increased expression of genes involved in these processes. This study demonstrates that starvation responses and biofilm formation are coregulated by <i>GTR1</i> and suggests that these responses are linked to compete with the microbiome for space and nutrients.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">29152581</PMID><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">2379-5042</ISSN><JournalIssue CitedMedium="Print"><Volume>2</Volume><Issue>6</Issue><PubDate><MedlineDate>2017 Nov-Dec</MedlineDate></PubDate></JournalIssue><Title>mSphere</Title><ISOAbbreviation>mSphere</ISOAbbreviation></Journal><ArticleTitle>The <i>Candida albicans</i> TOR-Activating GTPases Gtr1 and Rhb1 Coregulate Starvation Responses and Biofilm Formation.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e00477-17</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1128/mSphere.00477-17</ELocationID><Abstract><AbstractText>Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in eukaryotic cells and in the fungal pathogen <i>Candida albicans</i> regulates morphogenesis and nitrogen acquisition. Gtr1 encodes a highly conserved GTPase that in <i>Saccharomyces cerevisiae</i> regulates nitrogen sensing and TORC1 activation. Here, we characterize the role of <i>C. albicans GTR1</i> in TORC1 activation and compare it with the previously characterized GTPase Rhb1. A homozygous <i>gtr1/gtr1</i> mutant exhibited impaired TORC1-mediated phosphorylation of ribosomal protein S6 and increased susceptibility to rapamycin. Overexpression of <i>GTR1</i> impaired nitrogen starvation-induced filamentous growth, <i>MEP2</i> expression, and growth in bovine serum albumin as the sole nitrogen source. Both <i>GTR1</i> and <i>RHB1</i> were shown to regulate genes involved in ribosome biogenesis, amino acid biosynthesis, and expression of biofilm growth-induced genes. The <i>rhb1/rhb1</i> mutant exhibited a different pattern of expression of Sko1-regulated genes and increased susceptibility to Congo red and calcofluor white. The homozygous <i>gtr1/gtr1</i> mutant exhibited enhanced flocculation phenotypes and, similar to the <i>rhb1/rhb1</i> mutant, exhibited enhanced biofilm formation on plastic surfaces. In summary, Gtr1 and Rhb1 link nutrient sensing and biofilm formation and this connectivity may have evolved to enhance the competitiveness of <i>C. albicans</i> in niches where there is intense competition with other microbes for space and nutrients. <b>IMPORTANCE</b><i>Candida albicans</i> is the major fungal pathogen of humans and is responsible for a wide range of infections, including life-threatening systemic infections in susceptible hosts. Target of rapamycin complex 1 (TORC1) is an essential regulator of metabolism in this fungus, and components of this complex are under increased investigation as targets for new antifungal drugs. The present study characterized the role of <i>GTR1</i>, encoding a putative GTPase, in TORC1 activation. This study shows that <i>GTR1</i> encodes a protein required for activation of TORC1 activity in response to amino acids and regulation of nitrogen starvation responses. <i>GTR1</i> mutants show increased cell-cell adhesion and biofilm formation and increased expression of genes involved in these processes. This study demonstrates that starvation responses and biofilm formation are coregulated by <i>GTR1</i> and suggests that these responses are linked to compete with the microbiome for space and nutrients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Flanagan</LastName><ForeName>Peter R</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ning-Ning</ForeName><Initials>NN</Initials><AffiliationInfo><Affiliation>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fitzpatrick</LastName><ForeName>Darren J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hokamp</LastName><ForeName>Karsten</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>School of Genetics and Microbiology, University of Dublin, Trinity College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Köhler</LastName><ForeName>Julia R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moran</LastName><ForeName>Gary P</ForeName><Initials>GP</Initials><Identifier Source="ORCID">0000-0003-0469-1788</Identifier><AffiliationInfo><Affiliation>Division of Oral Biosciences, Dublin Dental University Hospital, University of Dublin, Trinity College Dublin, Dublin, Ireland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI095305</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI096054</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>11</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>mSphere</MedlineTA><NlmUniqueID>101674533</NlmUniqueID><ISSNLinking>2379-5042</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Candida albicans</Keyword><Keyword MajorTopicYN="N">TOR</Keyword><Keyword MajorTopicYN="N">biofilm</Keyword><Keyword MajorTopicYN="N">virulence</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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Flanagan</name></noRegion><name sortKey="Fitzpatrick, Darren J" sort="Fitzpatrick, Darren J" uniqKey="Fitzpatrick D" first="Darren J" last="Fitzpatrick">Darren J. Fitzpatrick</name><name sortKey="Hokamp, Karsten" sort="Hokamp, Karsten" uniqKey="Hokamp K" first="Karsten" last="Hokamp">Karsten Hokamp</name><name sortKey="Moran, Gary P" sort="Moran, Gary P" uniqKey="Moran G" first="Gary P" last="Moran">Gary P. Moran</name></country><country name="États-Unis"><region name="Massachusetts"><name sortKey="Liu, Ning Ning" sort="Liu, Ning Ning" uniqKey="Liu N" first="Ning-Ning" last="Liu">Ning-Ning Liu</name></region><name sortKey="Kohler, Julia R" sort="Kohler, Julia R" uniqKey="Kohler J" first="Julia R" last="Köhler">Julia R. Köhler</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:29152581
|texte= The Candida albicans TOR-Activating GTPases Gtr1 and Rhb1 Coregulate Starvation Responses and Biofilm Formation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:29152581" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |