RapamycinFungusV1, Main, Exploration, bibRecord, 000368

CpATG8, a Homolog of Yeast Autophagy Protein ATG8, Is Required for Pathogenesis and Hypovirus Accumulation in the Chest Blight Fungus.

Identifieur interne : 000368 ( Main/Exploration ); précédent : 000367; suivant : 000369

CpATG8, a Homolog of Yeast Autophagy Protein ATG8, Is Required for Pathogenesis and Hypovirus Accumulation in the Chest Blight Fungus.

Auteurs : Liming Shi [République populaire de Chine] ; Jinzi Wang [République populaire de Chine] ; Rui Quan [République populaire de Chine] ; Feng Yang [République populaire de Chine] ; Jinjie Shang [République populaire de Chine] ; Baoshan Chen [République populaire de Chine]

Source :

Frontiers in cellular and infection microbiology [ 2235-2988 ] ; 2019.

RBID : pubmed:31355148

Descripteurs français

KwdFr :
- ARN viral (génétique), ARN viral (métabolisme), Activation de la transcription (MeSH), Ascomycota (génétique), Ascomycota (métabolisme), Ascomycota (pathogénicité), Ascomycota (virologie), Autophagie (MeSH), Famille de la protéine-8 associée à l'autophagie (génétique), Famille de la protéine-8 associée à l'autophagie (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines fongiques (génétique), Protéines fongiques (métabolisme), Protéines virales (métabolisme), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (métabolisme), Thorax (microbiologie), Virulence (génétique).
MESH :
- génétique : ARN viral, Ascomycota, Famille de la protéine-8 associée à l'autophagie, Protéines de Saccharomyces cerevisiae, Protéines fongiques, Virulence.
- microbiologie : Thorax.
- métabolisme : ARN viral, Ascomycota, Famille de la protéine-8 associée à l'autophagie, Protéines fongiques, Protéines virales, Saccharomyces cerevisiae.
- pathogénicité : Ascomycota.
- virologie : Ascomycota.
- Activation de la transcription, Autophagie, Régulation de l'expression des gènes fongiques.

English descriptors

KwdEn :
- Ascomycota (genetics), Ascomycota (metabolism), Ascomycota (pathogenicity), Ascomycota (virology), Autophagy (MeSH), Autophagy-Related Protein 8 Family (genetics), Autophagy-Related Protein 8 Family (metabolism), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Regulation, Fungal (MeSH), RNA, Viral (genetics), RNA, Viral (metabolism), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Thorax (microbiology), Transcriptional Activation (MeSH), Viral Proteins (metabolism), Virulence (genetics).
MESH :
- chemical , genetics : Autophagy-Related Protein 8 Family, Fungal Proteins, RNA, Viral, Saccharomyces cerevisiae Proteins.
- genetics : Ascomycota, Virulence.
- metabolism : Ascomycota, Autophagy-Related Protein 8 Family, Fungal Proteins, RNA, Viral, Saccharomyces cerevisiae, Viral Proteins.
- microbiology : Thorax.
- pathogenicity : Ascomycota.
- virology : Ascomycota.
- Autophagy, Gene Expression Regulation, Fungal, Transcriptional Activation.

Abstract

Autophagy is a degradation system in the cell, involved in the turnover of cellular components, development, differentiation, immune responses, protection against pathogens, and cell death. Autophagy is induced by nutrient starvation, in which cytoplasmic components and organelles are digested via vacuoles/lysosomes. In this study, by using electron microscopy, we observed that hypovirus CHV1-EP713 infection of Cryphonectria parasitica, the causative agent of chestnut blight disease, caused proliferation of autophagic-like vesicles. This phenomenon could be mimicked by treating the wild-type strain of the fungus EP155 with the autophagy induction drug rapamycin. Some of the hypovirulence-associated traits, including reduced pigmentation and conidiation, were also observed in the rapamycin-treated EP155. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) revealed that genes involved in autophagy were up-regulated in expression. Deletion of cpatg8, a gene encoding a homolog of ATG8 in Saccharomyces cerevisiae, resulted in attenuation of virulence and reduction in sporulation, as well as accumulation of the double-stranded viral RNA. Furthermore, virus-encoded p29 protein was found to co-localize with CpATG8, implying that the viral protein may interfere with the function of CpATG8. Taken together, these findings show that cpatg8 can be regulated by the hypovirus and is required for virulence and development of the fungus and accumulation of viral dsRNA in chestnut blight fungus.

DOI: 10.3389/fcimb.2019.00222
PubMed: 31355148
PubMed Central: PMC6635641

Affiliations:

République populaire de Chine

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

to stream Main, to step Corpus: 000225
to stream Main, to step Curation: 000225

Le document en format XML

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<author><name sortKey="Yang, Feng" sort="Yang, Feng" uniqKey="Yang F" first="Feng" last="Yang">Feng Yang</name>
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<author><name sortKey="Chen, Baoshan" sort="Chen, Baoshan" uniqKey="Chen B" first="Baoshan" last="Chen">Baoshan Chen</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ascomycota (genetics)</term>
<term>Ascomycota (metabolism)</term>
<term>Ascomycota (pathogenicity)</term>
<term>Ascomycota (virology)</term>
<term>Autophagy (MeSH)</term>
<term>Autophagy-Related Protein 8 Family (genetics)</term>
<term>Autophagy-Related Protein 8 Family (metabolism)</term>
<term>Fungal Proteins (genetics)</term>
<term>Fungal Proteins (metabolism)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>RNA, Viral (genetics)</term>
<term>RNA, Viral (metabolism)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Thorax (microbiology)</term>
<term>Transcriptional Activation (MeSH)</term>
<term>Viral Proteins (metabolism)</term>
<term>Virulence (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral (génétique)</term>
<term>ARN viral (métabolisme)</term>
<term>Activation de la transcription (MeSH)</term>
<term>Ascomycota (génétique)</term>
<term>Ascomycota (métabolisme)</term>
<term>Ascomycota (pathogénicité)</term>
<term>Ascomycota (virologie)</term>
<term>Autophagie (MeSH)</term>
<term>Famille de la protéine-8 associée à l'autophagie (génétique)</term>
<term>Famille de la protéine-8 associée à l'autophagie (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines fongiques (génétique)</term>
<term>Protéines fongiques (métabolisme)</term>
<term>Protéines virales (métabolisme)</term>
<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Thorax (microbiologie)</term>
<term>Virulence (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 8 Family</term>
<term>Fungal Proteins</term>
<term>RNA, Viral</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Ascomycota</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN viral</term>
<term>Ascomycota</term>
<term>Famille de la protéine-8 associée à l'autophagie</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines fongiques</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Ascomycota</term>
<term>Autophagy-Related Protein 8 Family</term>
<term>Fungal Proteins</term>
<term>RNA, Viral</term>
<term>Saccharomyces cerevisiae</term>
<term>Viral Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Thorax</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Thorax</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN viral</term>
<term>Ascomycota</term>
<term>Famille de la protéine-8 associée à l'autophagie</term>
<term>Protéines fongiques</term>
<term>Protéines virales</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Ascomycota</term>
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<term>Gene Expression Regulation, Fungal</term>
<term>Transcriptional Activation</term>
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<front><div type="abstract" xml:lang="en">Autophagy is a degradation system in the cell, involved in the turnover of cellular components, development, differentiation, immune responses, protection against pathogens, and cell death. Autophagy is induced by nutrient starvation, in which cytoplasmic components and organelles are digested <i>via</i>
 vacuoles/lysosomes. In this study, by using electron microscopy, we observed that hypovirus CHV1-EP713 infection of <i>Cryphonectria parasitica</i>
, the causative agent of chestnut blight disease, caused proliferation of autophagic-like vesicles. This phenomenon could be mimicked by treating the wild-type strain of the fungus EP155 with the autophagy induction drug rapamycin. Some of the hypovirulence-associated traits, including reduced pigmentation and conidiation, were also observed in the rapamycin-treated EP155. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) revealed that genes involved in autophagy were up-regulated in expression. Deletion of <i>cpatg8</i>
, a gene encoding a homolog of ATG8 in <i>Saccharomyces cerevisiae</i>
, resulted in attenuation of virulence and reduction in sporulation, as well as accumulation of the double-stranded viral RNA. Furthermore, virus-encoded p29 protein was found to co-localize with CpATG8, implying that the viral protein may interfere with the function of CpATG8. Taken together, these findings show that <i>cpatg8</i>
 can be regulated by the hypovirus and is required for virulence and development of the fungus and accumulation of viral dsRNA in chestnut blight fungus.</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>02</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>09</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>9</Volume>
<PubDate><Year>2019</Year>
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<Title>Frontiers in cellular and infection microbiology</Title>
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</Journal>
<ArticleTitle>CpATG8, a Homolog of Yeast Autophagy Protein ATG8, Is Required for Pathogenesis and Hypovirus Accumulation in the Chest Blight Fungus.</ArticleTitle>
<Pagination><MedlinePgn>222</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.3389/fcimb.2019.00222</ELocationID>
<Abstract><AbstractText>Autophagy is a degradation system in the cell, involved in the turnover of cellular components, development, differentiation, immune responses, protection against pathogens, and cell death. Autophagy is induced by nutrient starvation, in which cytoplasmic components and organelles are digested <i>via</i>
 vacuoles/lysosomes. In this study, by using electron microscopy, we observed that hypovirus CHV1-EP713 infection of <i>Cryphonectria parasitica</i>
, the causative agent of chestnut blight disease, caused proliferation of autophagic-like vesicles. This phenomenon could be mimicked by treating the wild-type strain of the fungus EP155 with the autophagy induction drug rapamycin. Some of the hypovirulence-associated traits, including reduced pigmentation and conidiation, were also observed in the rapamycin-treated EP155. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) revealed that genes involved in autophagy were up-regulated in expression. Deletion of <i>cpatg8</i>
, a gene encoding a homolog of ATG8 in <i>Saccharomyces cerevisiae</i>
, resulted in attenuation of virulence and reduction in sporulation, as well as accumulation of the double-stranded viral RNA. Furthermore, virus-encoded p29 protein was found to co-localize with CpATG8, implying that the viral protein may interfere with the function of CpATG8. Taken together, these findings show that <i>cpatg8</i>
 can be regulated by the hypovirus and is required for virulence and development of the fungus and accumulation of viral dsRNA in chestnut blight fungus.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Liming</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jinzi</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Quan</LastName>
<ForeName>Rui</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Feng</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shang</LastName>
<ForeName>Jinjie</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Baoshan</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, College of Life Science and Technology, Guangxi University, Nanning, China.</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>07</Month>
<Day>10</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Front Cell Infect Microbiol</MedlineTA>
<NlmUniqueID>101585359</NlmUniqueID>
<ISSNLinking>2235-2988</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C113757">ATG8 protein, S cerevisiae</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071190">Autophagy-Related Protein 8 Family</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
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	Serveur d'exploration sur la rapamycine et les champignons
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CpATG8, a Homolog of Yeast Autophagy Protein ATG8, Is Required for Pathogenesis and Hypovirus Accumulation in the Chest Blight Fungus.

CpATG8, a Homolog of Yeast Autophagy Protein ATG8, Is Required for Pathogenesis and Hypovirus Accumulation in the Chest Blight Fungus.

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