GlutaredoxinV1, Main, Exploration, bibRecord, 000111

The monothiol glutaredoxin GrxD is essential for sensing iron starvation in Aspergillus fumigatus.

Identifieur interne : 000111 ( Main/Exploration ); précédent : 000110; suivant : 000112

The monothiol glutaredoxin GrxD is essential for sensing iron starvation in Aspergillus fumigatus.

Auteurs : Matthias Misslinger [Autriche] ; Mareike Thea Scheven [Allemagne] ; Peter Hortschansky [Allemagne] ; Manuel Sánchez L Pez-Berges [Autriche] ; Katharina Heiss [Autriche] ; Nicola Beckmann [Autriche] ; Thomas Heigl [Autriche] ; Martin Hermann [Autriche] ; Thomas Krüger [Allemagne] ; Olaf Kniemeyer [Allemagne] ; Axel A. Brakhage [Allemagne] ; Hubertus Haas [Autriche]

Source :

PLoS genetics [ 1553-7404 ] ; 2019.

RBID : pubmed:31525190

Descripteurs français

KwdFr :
- Aspergillus fumigatus (génétique), Aspergillus fumigatus (métabolisme), Facteurs de transcription (génétique), Fer (déficit), Fer (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Homéostasie (MeSH), Inanition (MeSH), Protéines fongiques (génétique), Régulation de l'expression des gènes fongiques (génétique), Virulence (MeSH).
MESH :
- déficit : Fer.
- génétique : Aspergillus fumigatus, Facteurs de transcription, Glutarédoxines, Protéines fongiques, Régulation de l'expression des gènes fongiques.
- métabolisme : Aspergillus fumigatus, Fer, Glutarédoxines.
- Homéostasie, Inanition, Virulence.

English descriptors

KwdEn :
- Aspergillus fumigatus (genetics), Aspergillus fumigatus (metabolism), Fungal Proteins (genetics), Gene Expression Regulation, Fungal (genetics), Glutaredoxins (genetics), Glutaredoxins (metabolism), Homeostasis (MeSH), Iron (deficiency), Iron (metabolism), Starvation (MeSH), Transcription Factors (genetics), Virulence (MeSH).
MESH :
- chemical , deficiency : Iron.
- chemical , genetics : Fungal Proteins, Glutaredoxins, Transcription Factors.
- genetics : Aspergillus fumigatus, Gene Expression Regulation, Fungal.
- metabolism : Aspergillus fumigatus, Glutaredoxins, Iron.
- Homeostasis, Starvation, Virulence.

Abstract

Efficient adaptation to iron starvation is an essential virulence determinant of the most common human mold pathogen, Aspergillus fumigatus. Here, we demonstrate that the cytosolic monothiol glutaredoxin GrxD plays an essential role in iron sensing in this fungus. Our studies revealed that (i) GrxD is essential for growth; (ii) expression of the encoding gene, grxD, is repressed by the transcription factor SreA in iron replete conditions and upregulated during iron starvation; (iii) during iron starvation but not iron sufficiency, GrxD displays predominant nuclear localization; (iv) downregulation of grxD expression results in de-repression of genes involved in iron-dependent pathways and repression of genes involved in iron acquisition during iron starvation, but did not significantly affect these genes during iron sufficiency; (v) GrxD displays protein-protein interaction with components of the cytosolic iron-sulfur cluster biosynthetic machinery, indicating a role in this process, and with the transcription factors SreA and HapX, which mediate iron regulation of iron acquisition and iron-dependent pathways; (vi) UV-Vis spectra of recombinant HapX or the complex of HapX and GrxD indicate coordination of iron-sulfur clusters; (vii) the cysteine required for iron-sulfur cluster coordination in GrxD is in vitro dispensable for interaction with HapX; and (viii) there is a GrxD-independent mechanism for sensing iron sufficiency by HapX; (ix) inactivation of SreA suppresses the lethal effect caused by GrxD inactivation. Taken together, this study demonstrates that GrxD is crucial for iron homeostasis in A. fumigatus.

DOI: 10.1371/journal.pgen.1008379
PubMed: 31525190
PubMed Central: PMC6762210

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="L Pez Berges, Manuel Sanchez" sort="L Pez Berges, Manuel Sanchez" uniqKey="L Pez Berges M" first="Manuel Sánchez" last="L Pez-Berges">Manuel Sánchez L Pez-Berges</name>
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<author><name sortKey="Heiss, Katharina" sort="Heiss, Katharina" uniqKey="Heiss K" first="Katharina" last="Heiss">Katharina Heiss</name>
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<author><name sortKey="Beckmann, Nicola" sort="Beckmann, Nicola" uniqKey="Beckmann N" first="Nicola" last="Beckmann">Nicola Beckmann</name>
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<author><name sortKey="Heigl, Thomas" sort="Heigl, Thomas" uniqKey="Heigl T" first="Thomas" last="Heigl">Thomas Heigl</name>
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<author><name sortKey="Hermann, Martin" sort="Hermann, Martin" uniqKey="Hermann M" first="Martin" last="Hermann">Martin Hermann</name>
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<author><name sortKey="Kruger, Thomas" sort="Kruger, Thomas" uniqKey="Kruger T" first="Thomas" last="Krüger">Thomas Krüger</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena</wicri:regionArea>
<wicri:noRegion>Jena</wicri:noRegion>
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<author><name sortKey="Kniemeyer, Olaf" sort="Kniemeyer, Olaf" uniqKey="Kniemeyer O" first="Olaf" last="Kniemeyer">Olaf Kniemeyer</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena</wicri:regionArea>
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<wicri:noRegion>Jena</wicri:noRegion>
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<author><name sortKey="Brakhage, Axel A" sort="Brakhage, Axel A" uniqKey="Brakhage A" first="Axel A" last="Brakhage">Axel A. Brakhage</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena</wicri:regionArea>
<wicri:noRegion>Jena</wicri:noRegion>
<wicri:noRegion>Jena</wicri:noRegion>
<wicri:noRegion>Jena</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Institute of Microbiology, Friedrich Schiller University Jena, Jena, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Institute of Microbiology, Friedrich Schiller University Jena, Jena</wicri:regionArea>
<wicri:noRegion>Jena</wicri:noRegion>
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<wicri:noRegion>Jena</wicri:noRegion>
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<author><name sortKey="Haas, Hubertus" sort="Haas, Hubertus" uniqKey="Haas H" first="Hubertus" last="Haas">Hubertus Haas</name>
<affiliation wicri:level="4"><nlm:affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</nlm:affiliation>
<country xml:lang="fr">Autriche</country>
<wicri:regionArea>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck</wicri:regionArea>
<orgName type="university">Université de médecine d'Innsbruck</orgName>
<placeName><settlement type="city">Innsbruck</settlement>
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<series><title level="j">PLoS genetics</title>
<idno type="eISSN">1553-7404</idno>
<imprint><date when="2019" type="published">2019</date>
</imprint>
</series>
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</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aspergillus fumigatus (genetics)</term>
<term>Aspergillus fumigatus (metabolism)</term>
<term>Fungal Proteins (genetics)</term>
<term>Gene Expression Regulation, Fungal (genetics)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Homeostasis (MeSH)</term>
<term>Iron (deficiency)</term>
<term>Iron (metabolism)</term>
<term>Starvation (MeSH)</term>
<term>Transcription Factors (genetics)</term>
<term>Virulence (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Aspergillus fumigatus (génétique)</term>
<term>Aspergillus fumigatus (métabolisme)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Fer (déficit)</term>
<term>Fer (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Homéostasie (MeSH)</term>
<term>Inanition (MeSH)</term>
<term>Protéines fongiques (génétique)</term>
<term>Régulation de l'expression des gènes fongiques (génétique)</term>
<term>Virulence (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Iron</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fungal Proteins</term>
<term>Glutaredoxins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Fer</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Aspergillus fumigatus</term>
<term>Gene Expression Regulation, Fungal</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Aspergillus fumigatus</term>
<term>Facteurs de transcription</term>
<term>Glutarédoxines</term>
<term>Protéines fongiques</term>
<term>Régulation de l'expression des gènes fongiques</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aspergillus fumigatus</term>
<term>Glutaredoxins</term>
<term>Iron</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Aspergillus fumigatus</term>
<term>Fer</term>
<term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Homeostasis</term>
<term>Starvation</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Homéostasie</term>
<term>Inanition</term>
<term>Virulence</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Efficient adaptation to iron starvation is an essential virulence determinant of the most common human mold pathogen, Aspergillus fumigatus. Here, we demonstrate that the cytosolic monothiol glutaredoxin GrxD plays an essential role in iron sensing in this fungus. Our studies revealed that (i) GrxD is essential for growth; (ii) expression of the encoding gene, grxD, is repressed by the transcription factor SreA in iron replete conditions and upregulated during iron starvation; (iii) during iron starvation but not iron sufficiency, GrxD displays predominant nuclear localization; (iv) downregulation of grxD expression results in de-repression of genes involved in iron-dependent pathways and repression of genes involved in iron acquisition during iron starvation, but did not significantly affect these genes during iron sufficiency; (v) GrxD displays protein-protein interaction with components of the cytosolic iron-sulfur cluster biosynthetic machinery, indicating a role in this process, and with the transcription factors SreA and HapX, which mediate iron regulation of iron acquisition and iron-dependent pathways; (vi) UV-Vis spectra of recombinant HapX or the complex of HapX and GrxD indicate coordination of iron-sulfur clusters; (vii) the cysteine required for iron-sulfur cluster coordination in GrxD is in vitro dispensable for interaction with HapX; and (viii) there is a GrxD-independent mechanism for sensing iron sufficiency by HapX; (ix) inactivation of SreA suppresses the lethal effect caused by GrxD inactivation. Taken together, this study demonstrates that GrxD is crucial for iron homeostasis in A. fumigatus.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31525190</PMID>
<DateCompleted><Year>2020</Year>
<Month>02</Month>
<Day>20</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>20</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>15</Volume>
<Issue>9</Issue>
<PubDate><Year>2019</Year>
<Month>09</Month>
</PubDate>
</JournalIssue>
<Title>PLoS genetics</Title>
<ISOAbbreviation>PLoS Genet</ISOAbbreviation>
</Journal>
<ArticleTitle>The monothiol glutaredoxin GrxD is essential for sensing iron starvation in Aspergillus fumigatus.</ArticleTitle>
<Pagination><MedlinePgn>e1008379</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1008379</ELocationID>
<Abstract><AbstractText>Efficient adaptation to iron starvation is an essential virulence determinant of the most common human mold pathogen, Aspergillus fumigatus. Here, we demonstrate that the cytosolic monothiol glutaredoxin GrxD plays an essential role in iron sensing in this fungus. Our studies revealed that (i) GrxD is essential for growth; (ii) expression of the encoding gene, grxD, is repressed by the transcription factor SreA in iron replete conditions and upregulated during iron starvation; (iii) during iron starvation but not iron sufficiency, GrxD displays predominant nuclear localization; (iv) downregulation of grxD expression results in de-repression of genes involved in iron-dependent pathways and repression of genes involved in iron acquisition during iron starvation, but did not significantly affect these genes during iron sufficiency; (v) GrxD displays protein-protein interaction with components of the cytosolic iron-sulfur cluster biosynthetic machinery, indicating a role in this process, and with the transcription factors SreA and HapX, which mediate iron regulation of iron acquisition and iron-dependent pathways; (vi) UV-Vis spectra of recombinant HapX or the complex of HapX and GrxD indicate coordination of iron-sulfur clusters; (vii) the cysteine required for iron-sulfur cluster coordination in GrxD is in vitro dispensable for interaction with HapX; and (viii) there is a GrxD-independent mechanism for sensing iron sufficiency by HapX; (ix) inactivation of SreA suppresses the lethal effect caused by GrxD inactivation. Taken together, this study demonstrates that GrxD is crucial for iron homeostasis in A. fumigatus.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Misslinger</LastName>
<ForeName>Matthias</ForeName>
<Initials>M</Initials>
<Identifier Source="ORCID">0000-0002-6380-700X</Identifier>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Scheven</LastName>
<ForeName>Mareike Thea</ForeName>
<Initials>MT</Initials>
<Identifier Source="ORCID">0000-0001-8618-3618</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Microbiology, Friedrich Schiller University Jena, Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hortschansky</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
<Identifier Source="ORCID">0000-0001-5194-9054</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>López-Berges</LastName>
<ForeName>Manuel Sánchez</ForeName>
<Initials>MS</Initials>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heiss</LastName>
<ForeName>Katharina</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beckmann</LastName>
<ForeName>Nicola</ForeName>
<Initials>N</Initials>
<Identifier Source="ORCID">0000-0003-4010-4384</Identifier>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heigl</LastName>
<ForeName>Thomas</ForeName>
<Initials>T</Initials>
<Identifier Source="ORCID">0000-0003-1571-8579</Identifier>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hermann</LastName>
<ForeName>Martin</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Anaesthesiology and Critical Care Medicine, Medical University of Innsbruck, Innsbruck, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Krüger</LastName>
<ForeName>Thomas</ForeName>
<Initials>T</Initials>
<Identifier Source="ORCID">0000-0001-8984-3853</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kniemeyer</LastName>
<ForeName>Olaf</ForeName>
<Initials>O</Initials>
<Identifier Source="ORCID">0000-0002-9493-6402</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brakhage</LastName>
<ForeName>Axel A</ForeName>
<Initials>AA</Initials>
<Identifier Source="ORCID">0000-0002-8814-4193</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Microbiology, Friedrich Schiller University Jena, Jena, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Haas</LastName>
<ForeName>Hubertus</ForeName>
<Initials>H</Initials>
<Identifier Source="ORCID">0000-0003-2472-9878</Identifier>
<AffiliationInfo><Affiliation>Institute of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.</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>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>09</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS Genet</MedlineTA>
<NlmUniqueID>101239074</NlmUniqueID>
<ISSNLinking>1553-7390</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance>
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<Chemical><RegistryNumber>E1UOL152H7</RegistryNumber>
<NameOfSubstance UI="D007501">Iron</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D001232" MajorTopicYN="N">Aspergillus fumigatus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013217" MajorTopicYN="N">Starvation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<CoiStatement>The authors have declared that no competing interests exist.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>03</Month>
<Day>04</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>08</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>09</Month>
<Day>26</Day>
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<Month>9</Month>
<Day>17</Day>
<Hour>6</Hour>
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<Month>2</Month>
<Day>23</Day>
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The monothiol glutaredoxin GrxD is essential for sensing iron starvation in Aspergillus fumigatus.

The monothiol glutaredoxin GrxD is essential for sensing iron starvation in Aspergillus fumigatus.

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