The overexpression of OsACBP5 protects transgenic rice against necrotrophic, hemibiotrophic and biotrophic pathogens.
Identifieur interne : 000015 ( Main/Exploration ); précédent : 000014; suivant : 000016The overexpression of OsACBP5 protects transgenic rice against necrotrophic, hemibiotrophic and biotrophic pathogens.
Auteurs : Saritha Panthapulakkal Narayanan [République populaire de Chine] ; Shiu-Cheung Lung [République populaire de Chine] ; Pan Liao [République populaire de Chine] ; Clive Lo [République populaire de Chine] ; Mee-Len Chye [République populaire de Chine]Source :
- Scientific reports [ 2045-2322 ] ; 2020.
Abstract
The most devastating diseases in rice (Oryza sativa) are sheath blight caused by the fungal necrotroph Rhizoctonia solani, rice blast by hemibiotrophic fungus Magnaporthe oryzae, and leaf blight by bacterial biotroph Xanthomonas oryzae (Xoo). It has been reported that the Class III acyl-CoA-binding proteins (ACBPs) such as those from dicots (Arabidopsis and grapevine) play a role in defence against biotrophic pathogens. Of the six Arabidopsis (Arabidopsis thaliana) ACBPs, AtACBP3 conferred protection in transgenic Arabidopsis against Pseudomonas syringae, but not the necrotrophic fungus, Botrytis cinerea. Similar to Arabidopsis, rice possesses six ACBPs, designated OsACBPs. The aims of this study were to test whether OsACBP5, the homologue of AtACBP3, can confer resistance against representative necrotrophic, hemibiotrophic and biotrophic phytopathogens and to understand the mechanisms in protection. Herein, when OsACBP5 was overexpressed in rice, the OsACBP5-overexpressing (OsACBP5-OE) lines exhibited enhanced disease resistance against representative necrotrophic (R. solani & Cercospora oryzae), hemibiotrophic (M. oryzae & Fusarium graminearum) and biotrophic (Xoo) phytopathogens. Progeny from a cross between OsACBP5-OE9 and the jasmonate (JA)-signalling deficient mutant were more susceptible than the wild type to infection by the necrotroph R. solani. In contrast, progeny from a cross between OsACBP5-OE9 and the salicylic acid (SA)-signalling deficient mutant was more susceptible to infection by the hemibiotroph M. oryzae and biotroph Xoo. Hence, enhanced resistance of OsACBP5-OEs against representative necrotrophs appears to be JA-dependent whilst that to (hemi)biotrophs is SA-mediated.
DOI: 10.1038/s41598-020-71851-9
PubMed: 32913218
PubMed Central: PMC7483469
Affiliations:
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uniqKey="Lo C" first="Clive" last="Lo">Clive Lo</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chye, Mee Len" sort="Chye, Mee Len" uniqKey="Chye M" first="Mee-Len" last="Chye">Mee-Len Chye</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China. mlchye@hku.hk.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong 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last="Panthapulakkal Narayanan">Saritha Panthapulakkal Narayanan</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Lung, Shiu Cheung" sort="Lung, Shiu Cheung" uniqKey="Lung S" first="Shiu-Cheung" last="Lung">Shiu-Cheung Lung</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Liao, Pan" sort="Liao, Pan" uniqKey="Liao P" first="Pan" last="Liao">Pan Liao</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Lo, Clive" sort="Lo, Clive" uniqKey="Lo C" first="Clive" last="Lo">Clive Lo</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author><author><name sortKey="Chye, Mee Len" sort="Chye, Mee Len" uniqKey="Chye M" first="Mee-Len" last="Chye">Mee-Len Chye</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China. mlchye@hku.hk.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong</wicri:regionArea><wicri:noRegion>Hong Kong</wicri:noRegion></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The most devastating diseases in rice (Oryza sativa) are sheath blight caused by the fungal necrotroph Rhizoctonia solani, rice blast by hemibiotrophic fungus Magnaporthe oryzae, and leaf blight by bacterial biotroph Xanthomonas oryzae (Xoo). It has been reported that the Class III acyl-CoA-binding proteins (ACBPs) such as those from dicots (Arabidopsis and grapevine) play a role in defence against biotrophic pathogens. Of the six Arabidopsis (Arabidopsis thaliana) ACBPs, AtACBP3 conferred protection in transgenic Arabidopsis against Pseudomonas syringae, but not the necrotrophic fungus, Botrytis cinerea. Similar to Arabidopsis, rice possesses six ACBPs, designated OsACBPs. The aims of this study were to test whether OsACBP5, the homologue of AtACBP3, can confer resistance against representative necrotrophic, hemibiotrophic and biotrophic phytopathogens and to understand the mechanisms in protection. Herein, when OsACBP5 was overexpressed in rice, the OsACBP5-overexpressing (OsACBP5-OE) lines exhibited enhanced disease resistance against representative necrotrophic (R. solani & Cercospora oryzae), hemibiotrophic (M. oryzae & Fusarium graminearum) and biotrophic (Xoo) phytopathogens. Progeny from a cross between OsACBP5-OE9 and the jasmonate (JA)-signalling deficient mutant were more susceptible than the wild type to infection by the necrotroph R. solani. In contrast, progeny from a cross between OsACBP5-OE9 and the salicylic acid (SA)-signalling deficient mutant was more susceptible to infection by the hemibiotroph M. oryzae and biotroph Xoo. Hence, enhanced resistance of OsACBP5-OEs against representative necrotrophs appears to be JA-dependent whilst that to (hemi)biotrophs is SA-mediated.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32913218</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>27</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>09</Month><Day>10</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>The overexpression of OsACBP5 protects transgenic rice against necrotrophic, hemibiotrophic and biotrophic pathogens.</ArticleTitle><Pagination><MedlinePgn>14918</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-020-71851-9</ELocationID><Abstract><AbstractText>The most devastating diseases in rice (Oryza sativa) are sheath blight caused by the fungal necrotroph Rhizoctonia solani, rice blast by hemibiotrophic fungus Magnaporthe oryzae, and leaf blight by bacterial biotroph Xanthomonas oryzae (Xoo). It has been reported that the Class III acyl-CoA-binding proteins (ACBPs) such as those from dicots (Arabidopsis and grapevine) play a role in defence against biotrophic pathogens. Of the six Arabidopsis (Arabidopsis thaliana) ACBPs, AtACBP3 conferred protection in transgenic Arabidopsis against Pseudomonas syringae, but not the necrotrophic fungus, Botrytis cinerea. Similar to Arabidopsis, rice possesses six ACBPs, designated OsACBPs. The aims of this study were to test whether OsACBP5, the homologue of AtACBP3, can confer resistance against representative necrotrophic, hemibiotrophic and biotrophic phytopathogens and to understand the mechanisms in protection. Herein, when OsACBP5 was overexpressed in rice, the OsACBP5-overexpressing (OsACBP5-OE) lines exhibited enhanced disease resistance against representative necrotrophic (R. solani & Cercospora oryzae), hemibiotrophic (M. oryzae & Fusarium graminearum) and biotrophic (Xoo) phytopathogens. Progeny from a cross between OsACBP5-OE9 and the jasmonate (JA)-signalling deficient mutant were more susceptible than the wild type to infection by the necrotroph R. solani. In contrast, progeny from a cross between OsACBP5-OE9 and the salicylic acid (SA)-signalling deficient mutant was more susceptible to infection by the hemibiotroph M. oryzae and biotroph Xoo. Hence, enhanced resistance of OsACBP5-OEs against representative necrotrophs appears to be JA-dependent whilst that to (hemi)biotrophs is SA-mediated.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Panthapulakkal Narayanan</LastName><ForeName>Saritha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lung</LastName><ForeName>Shiu-Cheung</ForeName><Initials>SC</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Pan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lo</LastName><ForeName>Clive</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chye</LastName><ForeName>Mee-Len</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Pokfulam, Hong Kong, China. mlchye@hku.hk.</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>2020</Year><Month>09</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci 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