RapamycinFungusV1, Main, Exploration, bibRecord, 000018

Transposon mobilization in the human fungal pathogen Cryptococcus is mutagenic during infection and promotes drug resistance in vitro.

Identifieur interne : 000018 ( Main/Exploration ); précédent : 000017; suivant : 000019

Transposon mobilization in the human fungal pathogen Cryptococcus is mutagenic during infection and promotes drug resistance in vitro.

Auteurs : Asiya Gusa [États-Unis] ; Jonathan D. Williams [États-Unis] ; Jang-Eun Cho [États-Unis] ; Anna Floyd Averette [États-Unis] ; Sheng Sun [États-Unis] ; Eva Mei Shouse [États-Unis] ; Joseph Heitman [États-Unis] ; J Andrew Alspaugh [États-Unis] ; Sue Jinks-Robertson [États-Unis]

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2020.

RBID : pubmed:32303657

Descripteurs français

KwdFr :
- Acide orotique (analogues et dérivés), Acide orotique (effets indésirables), Acide orotique (pharmacologie), Animaux (MeSH), Antifongiques (effets indésirables), Antifongiques (pharmacologie), Cryptococcus neoformans (effets des médicaments et des substances chimiques), Cryptococcus neoformans (pathogénicité), Humains (MeSH), Interactions hôte-pathogène (génétique), Mutagenèse (génétique), Mycoses (génétique), Mycoses (microbiologie), Résistance des champignons aux médicaments (génétique), Rétroéléments (génétique), Sirolimus (pharmacologie), Souris (MeSH), Tacrolimus (pharmacologie), Virulence (génétique).
MESH :
- analogues et dérivés : Acide orotique.
- effets des médicaments et des substances chimiques : Cryptococcus neoformans.
- effets indésirables : Acide orotique, Antifongiques.
- génétique : Interactions hôte-pathogène, Mutagenèse, Mycoses, Résistance des champignons aux médicaments, Rétroéléments, Virulence.
- microbiologie : Mycoses.
- pathogénicité : Cryptococcus neoformans.
- pharmacologie : Acide orotique, Antifongiques, Sirolimus, Tacrolimus.
- Animaux, Humains, Souris.

English descriptors

KwdEn :
- Animals (MeSH), Antifungal Agents (adverse effects), Antifungal Agents (pharmacology), Cryptococcus neoformans (drug effects), Cryptococcus neoformans (pathogenicity), Drug Resistance, Fungal (genetics), Host-Pathogen Interactions (genetics), Humans (MeSH), Mice (MeSH), Mutagenesis (genetics), Mycoses (genetics), Mycoses (microbiology), Orotic Acid (adverse effects), Orotic Acid (analogs & derivatives), Orotic Acid (pharmacology), Retroelements (genetics), Sirolimus (pharmacology), Tacrolimus (pharmacology), Virulence (genetics).
MESH :
- chemical , adverse effects : Antifungal Agents, Orotic Acid.
- chemical , analogs & derivatives : Orotic Acid.
- chemical , genetics : Retroelements.
- chemical , pharmacology : Antifungal Agents, Orotic Acid, Sirolimus, Tacrolimus.
- drug effects : Cryptococcus neoformans.
- genetics : Drug Resistance, Fungal, Host-Pathogen Interactions, Mutagenesis, Mycoses, Virulence.
- microbiology : Mycoses.
- pathogenicity : Cryptococcus neoformans.
- Animals, Humans, Mice.

Abstract

When transitioning from the environment, pathogenic microorganisms must adapt rapidly to survive in hostile host conditions. This is especially true for environmental fungi that cause opportunistic infections in immunocompromised patients since these microbes are not well adapted human pathogens. Cryptococcus species are yeastlike fungi that cause lethal infections, especially in HIV-infected patients. Using Cryptococcus deneoformans in a murine model of infection, we examined contributors to drug resistance and demonstrated that transposon mutagenesis drives the development of 5-fluoroorotic acid (5FOA) resistance. Inactivation of target genes URA3 or URA5 primarily reflected the insertion of two transposable elements (TEs): the T1 DNA transposon and the TCN12 retrotransposon. Consistent with in vivo results, increased rates of mutagenesis and resistance to 5FOA and the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluorocytosine (5FC) were found when Cryptococcus was incubated at 37° compared to 30° in vitro, a condition that mimics the temperature shift that occurs during the environment-to-host transition. Inactivation of the RNA interference (RNAi) pathway, which suppresses TE movement in many organisms, was not sufficient to elevate TE movement at 30° to the level observed at 37°. We propose that temperature-dependent TE mobilization in Cryptococcus is an important mechanism that enhances microbial adaptation and promotes pathogenesis and drug resistance in the human host.

DOI: 10.1073/pnas.2001451117
PubMed: 32303657
PubMed Central: PMC7211991

Affiliations:

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to stream Main, to step Corpus: 000090
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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antifungal Agents (adverse effects)</term>
<term>Antifungal Agents (pharmacology)</term>
<term>Cryptococcus neoformans (drug effects)</term>
<term>Cryptococcus neoformans (pathogenicity)</term>
<term>Drug Resistance, Fungal (genetics)</term>
<term>Host-Pathogen Interactions (genetics)</term>
<term>Humans (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mutagenesis (genetics)</term>
<term>Mycoses (genetics)</term>
<term>Mycoses (microbiology)</term>
<term>Orotic Acid (adverse effects)</term>
<term>Orotic Acid (analogs & derivatives)</term>
<term>Orotic Acid (pharmacology)</term>
<term>Retroelements (genetics)</term>
<term>Sirolimus (pharmacology)</term>
<term>Tacrolimus (pharmacology)</term>
<term>Virulence (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acide orotique (analogues et dérivés)</term>
<term>Acide orotique (effets indésirables)</term>
<term>Acide orotique (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Antifongiques (effets indésirables)</term>
<term>Antifongiques (pharmacologie)</term>
<term>Cryptococcus neoformans (effets des médicaments et des substances chimiques)</term>
<term>Cryptococcus neoformans (pathogénicité)</term>
<term>Humains (MeSH)</term>
<term>Interactions hôte-pathogène (génétique)</term>
<term>Mutagenèse (génétique)</term>
<term>Mycoses (génétique)</term>
<term>Mycoses (microbiologie)</term>
<term>Résistance des champignons aux médicaments (génétique)</term>
<term>Rétroéléments (génétique)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Tacrolimus (pharmacologie)</term>
<term>Virulence (génétique)</term>
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<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antifungal Agents</term>
<term>Orotic Acid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Orotic Acid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Retroelements</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antifungal Agents</term>
<term>Orotic Acid</term>
<term>Sirolimus</term>
<term>Tacrolimus</term>
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<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Acide orotique</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cryptococcus neoformans</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cryptococcus neoformans</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Acide orotique</term>
<term>Antifongiques</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drug Resistance, Fungal</term>
<term>Host-Pathogen Interactions</term>
<term>Mutagenesis</term>
<term>Mycoses</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interactions hôte-pathogène</term>
<term>Mutagenèse</term>
<term>Mycoses</term>
<term>Résistance des champignons aux médicaments</term>
<term>Rétroéléments</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Mycoses</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Mycoses</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Cryptococcus neoformans</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Cryptococcus neoformans</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide orotique</term>
<term>Antifongiques</term>
<term>Sirolimus</term>
<term>Tacrolimus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Mice</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Souris</term>
</keywords>
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<front><div type="abstract" xml:lang="en">When transitioning from the environment, pathogenic microorganisms must adapt rapidly to survive in hostile host conditions. This is especially true for environmental fungi that cause opportunistic infections in immunocompromised patients since these microbes are not well adapted human pathogens. <i>Cryptococcus</i>
 species are yeastlike fungi that cause lethal infections, especially in HIV-infected patients. Using <i>Cryptococcus deneoformans</i>
 in a murine model of infection, we examined contributors to drug resistance and demonstrated that transposon mutagenesis drives the development of 5-fluoroorotic acid (5FOA) resistance. Inactivation of target genes <i>URA3</i>
 or <i>URA5</i>
 primarily reflected the insertion of two transposable elements (TEs): the T1 DNA transposon and the TCN12 retrotransposon. Consistent with in vivo results, increased rates of mutagenesis and resistance to 5FOA and the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluorocytosine (5FC) were found when <i>Cryptococcus</i>
 was incubated at 37° compared to 30° in vitro, a condition that mimics the temperature shift that occurs during the environment-to-host transition. Inactivation of the RNA interference (RNAi) pathway, which suppresses TE movement in many organisms, was not sufficient to elevate TE movement at 30° to the level observed at 37°. We propose that temperature-dependent TE mobilization in <i>Cryptococcus</i>
 is an important mechanism that enhances microbial adaptation and promotes pathogenesis and drug resistance in the human host.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>07</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>18</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>117</Volume>
<Issue>18</Issue>
<PubDate><Year>2020</Year>
<Month>05</Month>
<Day>05</Day>
</PubDate>
</JournalIssue>
<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation>
</Journal>
<ArticleTitle>Transposon mobilization in the human fungal pathogen <i>Cryptococcus</i>
 is mutagenic during infection and promotes drug resistance in vitro.</ArticleTitle>
<Pagination><MedlinePgn>9973-9980</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.2001451117</ELocationID>
<Abstract><AbstractText>When transitioning from the environment, pathogenic microorganisms must adapt rapidly to survive in hostile host conditions. This is especially true for environmental fungi that cause opportunistic infections in immunocompromised patients since these microbes are not well adapted human pathogens. <i>Cryptococcus</i>
 species are yeastlike fungi that cause lethal infections, especially in HIV-infected patients. Using <i>Cryptococcus deneoformans</i>
 in a murine model of infection, we examined contributors to drug resistance and demonstrated that transposon mutagenesis drives the development of 5-fluoroorotic acid (5FOA) resistance. Inactivation of target genes <i>URA3</i>
 or <i>URA5</i>
 primarily reflected the insertion of two transposable elements (TEs): the T1 DNA transposon and the TCN12 retrotransposon. Consistent with in vivo results, increased rates of mutagenesis and resistance to 5FOA and the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluorocytosine (5FC) were found when <i>Cryptococcus</i>
 was incubated at 37° compared to 30° in vitro, a condition that mimics the temperature shift that occurs during the environment-to-host transition. Inactivation of the RNA interference (RNAi) pathway, which suppresses TE movement in many organisms, was not sufficient to elevate TE movement at 30° to the level observed at 37°. We propose that temperature-dependent TE mobilization in <i>Cryptococcus</i>
 is an important mechanism that enhances microbial adaptation and promotes pathogenesis and drug resistance in the human host.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gusa</LastName>
<ForeName>Asiya</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">0000-0001-9915-1834</Identifier>
<AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Williams</LastName>
<ForeName>Jonathan D</ForeName>
<Initials>JD</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710.</Affiliation>
</AffiliationInfo>
</Author>
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   |texte=   Transposon mobilization in the human fungal pathogen Cryptococcus is mutagenic during infection and promotes drug resistance in vitro.
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Transposon mobilization in the human fungal pathogen Cryptococcus is mutagenic during infection and promotes drug resistance in vitro.

Transposon mobilization in the human fungal pathogen Cryptococcus is mutagenic during infection and promotes drug resistance in vitro.

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