Natural mismatch repair mutations mediate phenotypic diversity and drug resistance in Cryptococcus deuterogattii.
Identifieur interne : 000789 ( Main/Exploration ); précédent : 000788; suivant : 000790Natural mismatch repair mutations mediate phenotypic diversity and drug resistance in Cryptococcus deuterogattii.
Auteurs : R Blake Billmyre [États-Unis] ; Shelly Applen Clancey [États-Unis] ; Joseph Heitman [États-Unis]Source :
- eLife [ 2050-084X ] ; 2017.
Descripteurs français
- KwdFr :
- Codon non-sens (MeSH), Cryptococcus (effets des médicaments et des substances chimiques), Cryptococcus (génétique), Cryptococcus (physiologie), Protéine-2 homologue de MutS (génétique), Protéines fongiques (génétique), Résistance des champignons aux médicaments (MeSH), Séquençage du génome entier (MeSH), Taux de mutation (MeSH), Variation intra-population (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Cryptococcus.
- génétique : Cryptococcus, Protéine-2 homologue de MutS, Protéines fongiques.
- physiologie : Cryptococcus.
- Codon non-sens, Résistance des champignons aux médicaments, Séquençage du génome entier, Taux de mutation, Variation intra-population.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Fungal Proteins, MutS Homolog 2 Protein.
- chemical : Codon, Nonsense.
- drug effects : Cryptococcus.
- genetics : Cryptococcus.
- physiology : Cryptococcus.
- Biological Variation, Population, Drug Resistance, Fungal, Mutation Rate, Whole Genome Sequencing.
Abstract
Pathogenic microbes confront an evolutionary conflict between the pressure to maintain genome stability and the need to adapt to mounting external stresses. Bacteria often respond with elevated mutation rates, but little evidence exists of stable eukaryotic hypermutators in nature. Whole genome resequencing of the human fungal pathogen Cryptococcus deuterogattii identified an outbreak lineage characterized by a nonsense mutation in the mismatch repair component MSH2. This defect results in a moderate mutation rate increase in typical genes, and a larger increase in genes containing homopolymer runs. This allows facile inactivation of genes with coding homopolymer runs including FRR1, which encodes the target of the immunosuppresive antifungal drugs FK506 and rapamycin. Our study identifies a eukaryotic hypermutator lineage spread over two continents and suggests that pathogenic eukaryotic microbes may experience similar selection pressures on mutation rate as bacterial pathogens, particularly during long periods of clonal growth or while expanding into new environments.
DOI: 10.7554/eLife.28802
PubMed: 28948913
PubMed Central: PMC5614558
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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xml:lang="en"><term>Biological Variation, Population (MeSH)</term><term>Codon, Nonsense (MeSH)</term><term>Cryptococcus (drug effects)</term><term>Cryptococcus (genetics)</term><term>Cryptococcus (physiology)</term><term>Drug Resistance, Fungal (MeSH)</term><term>Fungal Proteins (genetics)</term><term>MutS Homolog 2 Protein (genetics)</term><term>Mutation Rate (MeSH)</term><term>Whole Genome Sequencing (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Codon non-sens (MeSH)</term><term>Cryptococcus (effets des médicaments et des substances chimiques)</term><term>Cryptococcus (génétique)</term><term>Cryptococcus (physiologie)</term><term>Protéine-2 homologue de MutS (génétique)</term><term>Protéines fongiques (génétique)</term><term>Résistance des champignons aux médicaments (MeSH)</term><term>Séquençage du génome entier (MeSH)</term><term>Taux de mutation (MeSH)</term><term>Variation intra-population (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fungal Proteins</term><term>MutS Homolog 2 Protein</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Codon, Nonsense</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cryptococcus</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cryptococcus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cryptococcus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cryptococcus</term><term>Protéine-2 homologue de MutS</term><term>Protéines fongiques</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cryptococcus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cryptococcus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Biological Variation, Population</term><term>Drug Resistance, Fungal</term><term>Mutation Rate</term><term>Whole Genome Sequencing</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Codon non-sens</term><term>Résistance des champignons aux médicaments</term><term>Séquençage du génome entier</term><term>Taux de mutation</term><term>Variation intra-population</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pathogenic microbes confront an evolutionary conflict between the pressure to maintain genome stability and the need to adapt to mounting external stresses. Bacteria often respond with elevated mutation rates, but little evidence exists of stable eukaryotic hypermutators in nature. Whole genome resequencing of the human fungal pathogen <i>Cryptococcus deuterogattii</i> identified an outbreak lineage characterized by a nonsense mutation in the mismatch repair component <i>MSH2.</i> This defect results in a moderate mutation rate increase in typical genes, and a larger increase in genes containing homopolymer runs. This allows facile inactivation of genes with coding homopolymer runs including <i>FRR1</i>, which encodes the target of the immunosuppresive antifungal drugs FK506 and rapamycin. Our study identifies a eukaryotic hypermutator lineage spread over two continents and suggests that pathogenic eukaryotic microbes may experience similar selection pressures on mutation rate as bacterial pathogens, particularly during long periods of clonal growth or while expanding into new environments.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28948913</PMID><DateCompleted><Year>2018</Year><Month>06</Month><Day>13</Day></DateCompleted><DateRevised><Year>2019</Year><Month>01</Month><Day>24</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2050-084X</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><PubDate><Year>2017</Year><Month>09</Month><Day>26</Day></PubDate></JournalIssue><Title>eLife</Title><ISOAbbreviation>Elife</ISOAbbreviation></Journal><ArticleTitle>Natural mismatch repair mutations mediate phenotypic diversity and drug resistance in <i>Cryptococcus deuterogattii</i>.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.7554/eLife.28802</ELocationID><ELocationID EIdType="pii" ValidYN="Y">e28802</ELocationID><Abstract><AbstractText>Pathogenic microbes confront an evolutionary conflict between the pressure to maintain genome stability and the need to adapt to mounting external stresses. Bacteria often respond with elevated mutation rates, but little evidence exists of stable eukaryotic hypermutators in nature. Whole genome resequencing of the human fungal pathogen <i>Cryptococcus deuterogattii</i> identified an outbreak lineage characterized by a nonsense mutation in the mismatch repair component <i>MSH2.</i> This defect results in a moderate mutation rate increase in typical genes, and a larger increase in genes containing homopolymer runs. This allows facile inactivation of genes with coding homopolymer runs including <i>FRR1</i>, which encodes the target of the immunosuppresive antifungal drugs FK506 and rapamycin. Our study identifies a eukaryotic hypermutator lineage spread over two continents and suggests that pathogenic eukaryotic microbes may experience similar selection pressures on mutation rate as bacterial pathogens, particularly during long periods of clonal growth or while expanding into new environments.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Billmyre</LastName><ForeName>R Blake</ForeName><Initials>RB</Initials><Identifier Source="ORCID">0000-0003-4866-3711</Identifier><AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Duke University Medical Center, Durham, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clancey</LastName><ForeName>Shelly Applen</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Duke University Medical Center, Durham, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heitman</LastName><ForeName>Joseph</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Duke University Medical Center, Durham, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI039115</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI050113</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AI039115</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 GM007184</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType 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Population</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018389" MajorTopicYN="Y">Codon, Nonsense</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003454" MajorTopicYN="N">Cryptococcus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025141" MajorTopicYN="Y">Drug Resistance, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051718" MajorTopicYN="N">MutS Homolog 2 Protein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059645" MajorTopicYN="N">Mutation 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