Divergent targets of Aspergillus fumigatus AcuK and AcuM transcription factors during growth in vitro versus invasive disease.
Identifieur interne : 000504 ( PubMed/Corpus ); précédent : 000503; suivant : 000505Divergent targets of Aspergillus fumigatus AcuK and AcuM transcription factors during growth in vitro versus invasive disease.
Auteurs : Monsicha Pongpom ; Hong Liu ; Wenjie Xu ; Brendan D. Snarr ; Donald C. Sheppard ; Aaron P. Mitchell ; Scott G. FillerSource :
- Infection and immunity [ 1098-5522 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Aspergillosis (immunology), Aspergillosis (microbiology), Aspergillosis (pathology), Aspergillus fumigatus (genetics), Aspergillus fumigatus (growth & development), Aspergillus fumigatus (immunology), Aspergillus fumigatus (pathogenicity), Cortisone (administration & dosage), Cortisone (analogs & derivatives), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Deletion, Gene Expression Profiling, Gene Expression Regulation, Fungal, Gluconeogenesis (genetics), Immunocompromised Host, Iron (metabolism), Male, Mice, Mice, Inbred BALB C, Siderophores (metabolism), Transcription Factors (genetics), Transcription Factors (metabolism), Transcription, Genetic, Virulence.
- MESH :
- chemical , administration & dosage : Cortisone.
- chemical , analogs & derivatives : Cortisone.
- genetics : Aspergillus fumigatus, Fungal Proteins, Gluconeogenesis, Transcription Factors.
- growth & development : Aspergillus fumigatus.
- immunology : Aspergillosis, Aspergillus fumigatus.
- chemical , metabolism : Fungal Proteins, Iron, Siderophores, Transcription Factors.
- microbiology : Aspergillosis.
- pathogenicity : Aspergillus fumigatus.
- pathology : Aspergillosis.
- Animals, Gene Deletion, Gene Expression Profiling, Gene Expression Regulation, Fungal, Immunocompromised Host, Male, Mice, Mice, Inbred BALB C, Transcription, Genetic, Virulence.
Abstract
In Aspergillus nidulans, the AcuK and AcuM transcription factors form a complex that regulates gluconeogenesis. In Aspergillus fumigatus, AcuM governs gluconeogenesis and iron acquisition in vitro and virulence in immunosuppressed mice. However, the function of AcuK was previously unknown. Through in vitro studies, we found that A. fumigatus ΔacuK single and ΔacuK ΔacuM double mutants had impaired gluconeogenesis and iron acquisition, similar to the ΔacuM mutant. Also, the ΔacuK, ΔacuM, and ΔacuK ΔacuM mutants had similar virulence defects in mice. However, the ΔacuK mutant had a milder defect in extracellular siderophore activity and induction of epithelial cell damage in vitro than did the ΔacuM mutant. Moreover, overexpression of acuM in the ΔacuK mutant altered expression of 3 genes and partially restored growth under iron-limited conditions, suggesting that AcuM can govern some genes independently of AcuK. Although the ΔacuK and ΔacuM mutants had very similar transcriptional profiles in vitro, their transcriptional profiles during murine pulmonary infection differed both from their in vitro profiles and from each other. While AcuK and AcuM governed the expression of only a few iron-responsive genes in vivo, they influenced the expression of other virulence-related genes, such as hexA and dvrA. Therefore, in A. fumigatus, while AcuK and AcuM likely function as part of the same complex, they can also function independently of each other. Furthermore, AcuK and AcuM have different target genes in vivo than in vitro, suggesting that in vivo infection stimulates unique transcriptional regulatory pathways in A. fumigatus.
DOI: 10.1128/IAI.02685-14
PubMed: 25534941
Links to Exploration step
pubmed:25534941Le document en format XML
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Snarr</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Sheppard, Donald C" sort="Sheppard, Donald C" uniqKey="Sheppard D" first="Donald C" last="Sheppard">Donald C. Sheppard</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Mitchell, Aaron P" sort="Mitchell, Aaron P" uniqKey="Mitchell A" first="Aaron P" last="Mitchell">Aaron P. Mitchell</name><affiliation><nlm:affiliation>Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Filler, Scott G" sort="Filler, Scott G" uniqKey="Filler S" first="Scott G" last="Filler">Scott G. Filler</name><affiliation><nlm:affiliation>Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA David Geffen School of Medicine at UCLA, Los Angeles, California, USA sfiller@ucla.edu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25534941</idno><idno type="pmid">25534941</idno><idno type="doi">10.1128/IAI.02685-14</idno><idno type="wicri:Area/PubMed/Corpus">000504</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000504</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Divergent targets of Aspergillus fumigatus AcuK and AcuM transcription factors during growth in vitro versus invasive disease.</title><author><name sortKey="Pongpom, Monsicha" sort="Pongpom, Monsicha" uniqKey="Pongpom M" first="Monsicha" last="Pongpom">Monsicha Pongpom</name><affiliation><nlm:affiliation>Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Hong" sort="Liu, Hong" uniqKey="Liu H" first="Hong" last="Liu">Hong Liu</name><affiliation><nlm:affiliation>Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Xu, Wenjie" sort="Xu, Wenjie" uniqKey="Xu W" first="Wenjie" last="Xu">Wenjie Xu</name><affiliation><nlm:affiliation>Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Snarr, Brendan D" sort="Snarr, Brendan D" uniqKey="Snarr B" first="Brendan D" last="Snarr">Brendan D. Snarr</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Sheppard, Donald C" sort="Sheppard, Donald C" uniqKey="Sheppard D" first="Donald C" last="Sheppard">Donald C. Sheppard</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Mitchell, Aaron P" sort="Mitchell, Aaron P" uniqKey="Mitchell A" first="Aaron P" last="Mitchell">Aaron P. Mitchell</name><affiliation><nlm:affiliation>Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Filler, Scott G" sort="Filler, Scott G" uniqKey="Filler S" first="Scott G" last="Filler">Scott G. Filler</name><affiliation><nlm:affiliation>Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA David Geffen School of Medicine at UCLA, Los Angeles, California, USA sfiller@ucla.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Infection and immunity</title><idno type="eISSN">1098-5522</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Aspergillosis (immunology)</term><term>Aspergillosis (microbiology)</term><term>Aspergillosis (pathology)</term><term>Aspergillus fumigatus (genetics)</term><term>Aspergillus fumigatus (growth & development)</term><term>Aspergillus fumigatus (immunology)</term><term>Aspergillus fumigatus (pathogenicity)</term><term>Cortisone (administration & dosage)</term><term>Cortisone (analogs & derivatives)</term><term>Fungal Proteins (genetics)</term><term>Fungal Proteins (metabolism)</term><term>Gene Deletion</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation, Fungal</term><term>Gluconeogenesis (genetics)</term><term>Immunocompromised Host</term><term>Iron (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Siderophores (metabolism)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Transcription, Genetic</term><term>Virulence</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Cortisone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Cortisone</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Aspergillus fumigatus</term><term>Fungal Proteins</term><term>Gluconeogenesis</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Aspergillus fumigatus</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aspergillosis</term><term>Aspergillus fumigatus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fungal Proteins</term><term>Iron</term><term>Siderophores</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Aspergillosis</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Aspergillus fumigatus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aspergillosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gene Deletion</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation, Fungal</term><term>Immunocompromised Host</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Transcription, Genetic</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In Aspergillus nidulans, the AcuK and AcuM transcription factors form a complex that regulates gluconeogenesis. In Aspergillus fumigatus, AcuM governs gluconeogenesis and iron acquisition in vitro and virulence in immunosuppressed mice. However, the function of AcuK was previously unknown. Through in vitro studies, we found that A. fumigatus ΔacuK single and ΔacuK ΔacuM double mutants had impaired gluconeogenesis and iron acquisition, similar to the ΔacuM mutant. Also, the ΔacuK, ΔacuM, and ΔacuK ΔacuM mutants had similar virulence defects in mice. However, the ΔacuK mutant had a milder defect in extracellular siderophore activity and induction of epithelial cell damage in vitro than did the ΔacuM mutant. Moreover, overexpression of acuM in the ΔacuK mutant altered expression of 3 genes and partially restored growth under iron-limited conditions, suggesting that AcuM can govern some genes independently of AcuK. Although the ΔacuK and ΔacuM mutants had very similar transcriptional profiles in vitro, their transcriptional profiles during murine pulmonary infection differed both from their in vitro profiles and from each other. While AcuK and AcuM governed the expression of only a few iron-responsive genes in vivo, they influenced the expression of other virulence-related genes, such as hexA and dvrA. Therefore, in A. fumigatus, while AcuK and AcuM likely function as part of the same complex, they can also function independently of each other. Furthermore, AcuK and AcuM have different target genes in vivo than in vitro, suggesting that in vivo infection stimulates unique transcriptional regulatory pathways in A. fumigatus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25534941</PMID><DateCreated><Year>2015</Year><Month>02</Month><Day>14</Day></DateCreated><DateCompleted><Year>2015</Year><Month>04</Month><Day>13</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5522</ISSN><JournalIssue CitedMedium="Internet"><Volume>83</Volume><Issue>3</Issue><PubDate><Year>2015</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Divergent targets of Aspergillus fumigatus AcuK and AcuM transcription factors during growth in vitro versus invasive disease.</ArticleTitle><Pagination><MedlinePgn>923-33</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/IAI.02685-14</ELocationID><Abstract><AbstractText>In Aspergillus nidulans, the AcuK and AcuM transcription factors form a complex that regulates gluconeogenesis. In Aspergillus fumigatus, AcuM governs gluconeogenesis and iron acquisition in vitro and virulence in immunosuppressed mice. However, the function of AcuK was previously unknown. Through in vitro studies, we found that A. fumigatus ΔacuK single and ΔacuK ΔacuM double mutants had impaired gluconeogenesis and iron acquisition, similar to the ΔacuM mutant. Also, the ΔacuK, ΔacuM, and ΔacuK ΔacuM mutants had similar virulence defects in mice. However, the ΔacuK mutant had a milder defect in extracellular siderophore activity and induction of epithelial cell damage in vitro than did the ΔacuM mutant. Moreover, overexpression of acuM in the ΔacuK mutant altered expression of 3 genes and partially restored growth under iron-limited conditions, suggesting that AcuM can govern some genes independently of AcuK. Although the ΔacuK and ΔacuM mutants had very similar transcriptional profiles in vitro, their transcriptional profiles during murine pulmonary infection differed both from their in vitro profiles and from each other. While AcuK and AcuM governed the expression of only a few iron-responsive genes in vivo, they influenced the expression of other virulence-related genes, such as hexA and dvrA. Therefore, in A. fumigatus, while AcuK and AcuM likely function as part of the same complex, they can also function independently of each other. Furthermore, AcuK and AcuM have different target genes in vivo than in vitro, suggesting that in vivo infection stimulates unique transcriptional regulatory pathways in A. fumigatus.</AbstractText><CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pongpom</LastName><ForeName>Monsicha</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Hong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Wenjie</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Snarr</LastName><ForeName>Brendan D</ForeName><Initials>BD</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sheppard</LastName><ForeName>Donald C</ForeName><Initials>DC</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology and Department of Medicine, McGill University, Montreal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mitchell</LastName><ForeName>Aaron P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Filler</LastName><ForeName>Scott G</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA David Geffen School of Medicine at UCLA, Los Angeles, California, USA sfiller@ucla.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI30041</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R56AI111836</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01AI073829</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R56 AI111836</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI073829</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>12</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017262">Siderophores</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>883WKN7W8X</RegistryNumber><NameOfSubstance UI="C015087">cortisone acetate</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>V27W9254FZ</RegistryNumber><NameOfSubstance UI="D003348">Cortisone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>BMC Infect Dis. 2013;13:29</RefSource><PMID Version="1">23343366</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Anal Biochem. 1987 Jan;160(1):47-56</RefSource><PMID Version="1">2952030</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Microbiol. 2010 Nov;78(4):1038-54</RefSource><PMID Version="1">21062375</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eukaryot Cell. 2007 Dec;6(12):2437-47</RefSource><PMID Version="1">17921348</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Biol Cell. 2005 Dec;16(12):5866-79</RefSource><PMID Version="1">16207816</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Clin Infect Dis. 2009 Feb 1;48(3):265-73</RefSource><PMID 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Version="1">22347220</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Genet. 1998 May;33(5):378-85</RefSource><PMID Version="1">9618589</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Clin Microbiol Rev. 1999 Apr;12(2):310-50</RefSource><PMID Version="1">10194462</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001228" MajorTopicYN="N">Aspergillosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001232" MajorTopicYN="N">Aspergillus fumigatus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003348" MajorTopicYN="N">Cortisone</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="Y">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005943" MajorTopicYN="N">Gluconeogenesis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016867" MajorTopicYN="Y">Immunocompromised Host</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017262" MajorTopicYN="N">Siderophores</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4333448</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>4</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25534941</ArticleId><ArticleId IdType="pii">IAI.02685-14</ArticleId><ArticleId IdType="doi">10.1128/IAI.02685-14</ArticleId><ArticleId IdType="pmc">PMC4333448</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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