Cherry picking by pseudomonads: After a century of research on canker, genomics provides insights into the evolution of pathogenicity towards stone fruits.
Identifieur interne : 000200 ( Main/Exploration ); précédent : 000199; suivant : 000201Cherry picking by pseudomonads: After a century of research on canker, genomics provides insights into the evolution of pathogenicity towards stone fruits.
Auteurs : Michelle T. Hulin ; Robert W. Jackson ; Richard J. Harrison ; John W. MansfieldSource :
- Plant pathology [ 0032-0862 ] ; 2020.
Abstract
Bacterial canker disease is a major limiting factor in the growing of cherry and other Prunus species worldwide. At least five distinct clades within the bacterial species complex Pseudomonas syringae are known to be causal agents of the disease. The different pathogens commonly coexist in the field. Reducing canker is a challenging prospect as the efficacy of chemical controls and host resistance may vary against each of the diverse clades involved. Genomic analysis has revealed that the pathogens use a variable repertoire of virulence factors to cause the disease. Significantly, strains of P. syringae pv. syringae possess more genes for toxin biosynthesis and fewer encoding type III effector proteins. There is also a shared pool of key effector genes present on mobile elements such as plasmids and prophages that may have roles in virulence. By contrast, there is evidence that absence or truncation of certain effector genes, such as hopAB, is characteristic of cherry pathogens. Here we highlight how recent research, underpinned by the earlier epidemiological studies, is allowing significant progress in our understanding of the canker pathogens. This fundamental knowledge, combined with emerging insights into host genetics, provides the groundwork for development of precise control measures and informed approaches to breed for disease resistance.
DOI: 10.1111/ppa.13189
PubMed: 32742023
PubMed Central: PMC7386918
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cherry picking by pseudomonads: After a century of research on canker, genomics provides insights into the evolution of pathogenicity towards stone fruits.</title><author><name sortKey="Hulin, Michelle T" sort="Hulin, Michelle T" uniqKey="Hulin M" first="Michelle T" last="Hulin">Michelle T. Hulin</name><affiliation><nlm:affiliation>NIAB EMR East Malling UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB EMR East Malling UK.</wicri:noCountry></affiliation></author><author><name sortKey="Jackson, Robert W" sort="Jackson, Robert W" uniqKey="Jackson R" first="Robert W" last="Jackson">Robert W. Jackson</name><affiliation><nlm:affiliation>Birmingham Institute of Forest Research (BIFoR), University of Birmingham Birmingham UK.</nlm:affiliation><wicri:noCountry code="subField">University of Birmingham Birmingham UK</wicri:noCountry></affiliation><affiliation><nlm:affiliation>School of Biosciences, University of Birmingham Birmingham UK.</nlm:affiliation><wicri:noCountry code="subField">University of Birmingham Birmingham UK</wicri:noCountry></affiliation></author><author><name sortKey="Harrison, Richard J" sort="Harrison, Richard J" uniqKey="Harrison R" first="Richard J" last="Harrison">Richard J. Harrison</name><affiliation><nlm:affiliation>NIAB EMR East Malling UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB EMR East Malling UK.</wicri:noCountry></affiliation><affiliation><nlm:affiliation>NIAB Cambridge UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB Cambridge UK.</wicri:noCountry></affiliation></author><author><name sortKey="Mansfield, John W" sort="Mansfield, John W" uniqKey="Mansfield J" first="John W" last="Mansfield">John W. Mansfield</name><affiliation><nlm:affiliation>Faculty of Natural Sciences Imperial College London London UK.</nlm:affiliation><wicri:noCountry code="no comma">Faculty of Natural Sciences Imperial College London London UK.</wicri:noCountry></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32742023</idno><idno type="pmid">32742023</idno><idno type="doi">10.1111/ppa.13189</idno><idno type="pmc">PMC7386918</idno><idno type="wicri:Area/Main/Corpus">000165</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000165</idno><idno type="wicri:Area/Main/Curation">000165</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000165</idno><idno type="wicri:Area/Main/Exploration">000165</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cherry picking by pseudomonads: After a century of research on canker, genomics provides insights into the evolution of pathogenicity towards stone fruits.</title><author><name sortKey="Hulin, Michelle T" sort="Hulin, Michelle T" uniqKey="Hulin M" first="Michelle T" last="Hulin">Michelle T. Hulin</name><affiliation><nlm:affiliation>NIAB EMR East Malling UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB EMR East Malling UK.</wicri:noCountry></affiliation></author><author><name sortKey="Jackson, Robert W" sort="Jackson, Robert W" uniqKey="Jackson R" first="Robert W" last="Jackson">Robert W. Jackson</name><affiliation><nlm:affiliation>Birmingham Institute of Forest Research (BIFoR), University of Birmingham Birmingham UK.</nlm:affiliation><wicri:noCountry code="subField">University of Birmingham Birmingham UK</wicri:noCountry></affiliation><affiliation><nlm:affiliation>School of Biosciences, University of Birmingham Birmingham UK.</nlm:affiliation><wicri:noCountry code="subField">University of Birmingham Birmingham UK</wicri:noCountry></affiliation></author><author><name sortKey="Harrison, Richard J" sort="Harrison, Richard J" uniqKey="Harrison R" first="Richard J" last="Harrison">Richard J. Harrison</name><affiliation><nlm:affiliation>NIAB EMR East Malling UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB EMR East Malling UK.</wicri:noCountry></affiliation><affiliation><nlm:affiliation>NIAB Cambridge UK.</nlm:affiliation><wicri:noCountry code="no comma">NIAB Cambridge UK.</wicri:noCountry></affiliation></author><author><name sortKey="Mansfield, John W" sort="Mansfield, John W" uniqKey="Mansfield J" first="John W" last="Mansfield">John W. Mansfield</name><affiliation><nlm:affiliation>Faculty of Natural Sciences Imperial College London London UK.</nlm:affiliation><wicri:noCountry code="no comma">Faculty of Natural Sciences Imperial College London London UK.</wicri:noCountry></affiliation></author></analytic><series><title level="j">Plant pathology</title><idno type="ISSN">0032-0862</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">Bacterial canker disease is a major limiting factor in the growing of cherry and other <i>Prunus</i> species worldwide. At least five distinct clades within the bacterial species complex <i>Pseudomonas syringae</i> are known to be causal agents of the disease. The different pathogens commonly coexist in the field. Reducing canker is a challenging prospect as the efficacy of chemical controls and host resistance may vary against each of the diverse clades involved. Genomic analysis has revealed that the pathogens use a variable repertoire of virulence factors to cause the disease. Significantly, strains of <i>P</i>. <i>syringae</i> pv. <i>syringae</i> possess more genes for toxin biosynthesis and fewer encoding type III effector proteins. There is also a shared pool of key effector genes present on mobile elements such as plasmids and prophages that may have roles in virulence. By contrast, there is evidence that absence or truncation of certain effector genes, such as <i>hopAB</i>, is characteristic of cherry pathogens. Here we highlight how recent research, underpinned by the earlier epidemiological studies, is allowing significant progress in our understanding of the canker pathogens. This fundamental knowledge, combined with emerging insights into host genetics, provides the groundwork for development of precise control measures and informed approaches to breed for disease resistance.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32742023</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>28</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0032-0862</ISSN><JournalIssue CitedMedium="Print"><Volume>69</Volume><Issue>6</Issue><PubDate><Year>2020</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Plant pathology</Title><ISOAbbreviation>Plant Pathol</ISOAbbreviation></Journal><ArticleTitle>Cherry picking by pseudomonads: After a century of research on canker, genomics provides insights into the evolution of pathogenicity towards stone fruits.</ArticleTitle><Pagination><MedlinePgn>962-978</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/ppa.13189</ELocationID><Abstract><AbstractText>Bacterial canker disease is a major limiting factor in the growing of cherry and other <i>Prunus</i> species worldwide. At least five distinct clades within the bacterial species complex <i>Pseudomonas syringae</i> are known to be causal agents of the disease. The different pathogens commonly coexist in the field. Reducing canker is a challenging prospect as the efficacy of chemical controls and host resistance may vary against each of the diverse clades involved. Genomic analysis has revealed that the pathogens use a variable repertoire of virulence factors to cause the disease. Significantly, strains of <i>P</i>. <i>syringae</i> pv. <i>syringae</i> possess more genes for toxin biosynthesis and fewer encoding type III effector proteins. There is also a shared pool of key effector genes present on mobile elements such as plasmids and prophages that may have roles in virulence. By contrast, there is evidence that absence or truncation of certain effector genes, such as <i>hopAB</i>, is characteristic of cherry pathogens. Here we highlight how recent research, underpinned by the earlier epidemiological studies, is allowing significant progress in our understanding of the canker pathogens. This fundamental knowledge, combined with emerging insights into host genetics, provides the groundwork for development of precise control measures and informed approaches to breed for disease resistance.</AbstractText><CopyrightInformation>© 2020 The Authors. Plant Pathology published by John Wiley & Sons Ltd on behalf of British Society for Plant Pathology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hulin</LastName><ForeName>Michelle T</ForeName><Initials>MT</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-4240-5746</Identifier><AffiliationInfo><Affiliation>NIAB EMR East Malling UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jackson</LastName><ForeName>Robert W</ForeName><Initials>RW</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-2042-4105</Identifier><AffiliationInfo><Affiliation>Birmingham Institute of Forest Research (BIFoR), University of Birmingham Birmingham UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Biosciences, University of Birmingham Birmingham UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harrison</LastName><ForeName>Richard J</ForeName><Initials>RJ</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-3307-3519</Identifier><AffiliationInfo><Affiliation>NIAB EMR East Malling UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>NIAB Cambridge UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mansfield</LastName><ForeName>John W</ForeName><Initials>JW</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-0135-5140</Identifier><AffiliationInfo><Affiliation>Faculty of Natural Sciences Imperial College London London UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Plant Pathol</MedlineTA><NlmUniqueID>9883944</NlmUniqueID><ISSNLinking>0032-0862</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Prunus</Keyword><Keyword MajorTopicYN="N">Pseudomonas</Keyword><Keyword MajorTopicYN="N">evolution</Keyword><Keyword MajorTopicYN="N">pathogenicity</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>12</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>03</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>03</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>4</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32742023</ArticleId><ArticleId IdType="doi">10.1111/ppa.13189</ArticleId><ArticleId IdType="pii">PPA13189</ArticleId><ArticleId IdType="pmc">PMC7386918</ArticleId></ArticleIdList><pmc-dir>pmcsd</pmc-dir>
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IdType="pubmed">30781059</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Harrison, Richard J" sort="Harrison, Richard J" uniqKey="Harrison R" first="Richard J" last="Harrison">Richard J. 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