AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit.
Identifieur interne : 000210 ( Main/Exploration ); précédent : 000209; suivant : 000211AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit.
Auteurs : Jay Jayaraman [Nouvelle-Zélande] ; Minsoo Yoon [Nouvelle-Zélande] ; Emma R. Applegate [Nouvelle-Zélande] ; Erin A. Stroud [Nouvelle-Zélande] ; Matthew D. Templeton [Nouvelle-Zélande]Source :
- Molecular plant pathology [ 1364-3703 ] ; 2020.
Abstract
Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1-triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.
DOI: 10.1111/mpp.12989
PubMed: 32969167
PubMed Central: PMC7548996
Affiliations:
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Stroud</name><affiliation wicri:level="1"><nlm:affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</nlm:affiliation><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>The New Zealand Institute for Plant and Food Research Limited, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, University of Auckland, Auckland, New Zealand.</nlm:affiliation><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, University of Auckland, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="Templeton, Matthew D" sort="Templeton, Matthew D" uniqKey="Templeton M" first="Matthew D" last="Templeton">Matthew D. Templeton</name><affiliation wicri:level="1"><nlm:affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</nlm:affiliation><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>The New Zealand Institute for Plant and Food Research Limited, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Bio-Protection Research Centre, Lincoln, New Zealand.</nlm:affiliation><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Bio-Protection Research Centre, Lincoln</wicri:regionArea><wicri:noRegion>Lincoln</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, University of Auckland, Auckland, New Zealand.</nlm:affiliation><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, University of Auckland, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular plant pathology</title><idno type="eISSN">1364-3703</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">Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1-triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">32969167</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1364-3703</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>11</Issue><PubDate><Year>2020</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Molecular plant pathology</Title><ISOAbbreviation>Mol Plant Pathol</ISOAbbreviation></Journal><ArticleTitle>AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit.</ArticleTitle><Pagination><MedlinePgn>1467-1480</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/mpp.12989</ELocationID><Abstract><AbstractText>Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1-triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.</AbstractText><CopyrightInformation>© 2020 The Authors. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jayaraman</LastName><ForeName>Jay</ForeName><Initials>J</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-4959-9467</Identifier><AffiliationInfo><Affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Bio-Protection Research Centre, Lincoln, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yoon</LastName><ForeName>Minsoo</ForeName><Initials>M</Initials><Identifier Source="ORCID">https://orcid.org/0000-0001-5524-3972</Identifier><AffiliationInfo><Affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Applegate</LastName><ForeName>Emma R</ForeName><Initials>ER</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-3284-0066</Identifier><AffiliationInfo><Affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biological Sciences, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stroud</LastName><ForeName>Erin A</ForeName><Initials>EA</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-7900-4279</Identifier><AffiliationInfo><Affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biological Sciences, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Templeton</LastName><ForeName>Matthew D</ForeName><Initials>MD</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-0192-9041</Identifier><AffiliationInfo><Affiliation>The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Bio-Protection Research Centre, Lincoln, New Zealand.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biological Sciences, University of Auckland, Auckland, New Zealand.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Bio-Protection Research Centre</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Mol Plant Pathol</MedlineTA><NlmUniqueID>100954969</NlmUniqueID><ISSNLinking>1364-3703</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Pseudomonas syringae pv. actinidiae</Keyword><Keyword MajorTopicYN="N">avirulence</Keyword><Keyword MajorTopicYN="N">bacterial effcetors</Keyword><Keyword MajorTopicYN="N">effector knockout</Keyword><Keyword MajorTopicYN="N">kiwifruit</Keyword><Keyword MajorTopicYN="N">type III seceretion system</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>07</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>08</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Applegate</name><name sortKey="Applegate, Emma R" sort="Applegate, Emma R" uniqKey="Applegate E" first="Emma R" last="Applegate">Emma R. Applegate</name><name sortKey="Jayaraman, Jay" sort="Jayaraman, Jay" uniqKey="Jayaraman J" first="Jay" last="Jayaraman">Jay Jayaraman</name><name sortKey="Stroud, Erin A" sort="Stroud, Erin A" uniqKey="Stroud E" first="Erin A" last="Stroud">Erin A. Stroud</name><name sortKey="Stroud, Erin A" sort="Stroud, Erin A" uniqKey="Stroud E" first="Erin A" last="Stroud">Erin A. Stroud</name><name sortKey="Templeton, Matthew D" sort="Templeton, Matthew D" uniqKey="Templeton M" first="Matthew D" last="Templeton">Matthew D. Templeton</name><name sortKey="Templeton, Matthew D" sort="Templeton, Matthew D" uniqKey="Templeton M" first="Matthew D" last="Templeton">Matthew D. Templeton</name><name sortKey="Templeton, Matthew D" sort="Templeton, Matthew D" uniqKey="Templeton M" first="Matthew D" last="Templeton">Matthew D. Templeton</name><name sortKey="Yoon, Minsoo" sort="Yoon, Minsoo" uniqKey="Yoon M" first="Minsoo" last="Yoon">Minsoo Yoon</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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