Molecular determinants of resistance activation and suppression by Phytophthora infestans effector IPI-O.
Identifieur interne : 000230 ( Main/Exploration ); précédent : 000229; suivant : 000231Molecular determinants of resistance activation and suppression by Phytophthora infestans effector IPI-O.
Auteurs : Yu Chen [États-Unis] ; Zhenyu Liu ; Dennis A. HaltermanSource :
- PLoS pathogens [ 1553-7374 ] ; 2012.
Descripteurs français
- KwdFr :
- Gènes de plante (génétique), Immunité innée (génétique), Immunité innée (immunologie), Interactions hôte-pathogène (génétique), Maladies des plantes (génétique), Maladies des plantes (immunologie), Phytophthora infestans (génétique), Phytophthora infestans (métabolisme), Phytophthora infestans (pathogénicité), Régulation de l'expression des gènes végétaux (MeSH), Résistance à la maladie (génétique), Résistance à la maladie (immunologie).
- MESH :
- génétique : Gènes de plante, Immunité innée, Interactions hôte-pathogène, Maladies des plantes, Phytophthora infestans, Résistance à la maladie.
- immunologie : Immunité innée, Maladies des plantes, Résistance à la maladie.
- métabolisme : Phytophthora infestans.
- pathogénicité : Phytophthora infestans.
- Régulation de l'expression des gènes végétaux.
English descriptors
- KwdEn :
- Disease Resistance (genetics), Disease Resistance (immunology), Gene Expression Regulation, Plant (MeSH), Genes, Plant (genetics), Host-Pathogen Interactions (genetics), Immunity, Innate (genetics), Immunity, Innate (immunology), Phytophthora infestans (genetics), Phytophthora infestans (metabolism), Phytophthora infestans (pathogenicity), Plant Diseases (genetics), Plant Diseases (immunology).
- MESH :
- genetics : Disease Resistance, Genes, Plant, Host-Pathogen Interactions, Immunity, Innate, Phytophthora infestans, Plant Diseases.
- immunology : Disease Resistance, Immunity, Innate, Plant Diseases.
- metabolism : Phytophthora infestans.
- pathogenicity : Phytophthora infestans.
- Gene Expression Regulation, Plant.
Abstract
Despite intensive breeding efforts, potato late blight, caused by the oomycete pathogen Phytophthora infestans, remains a threat to potato production worldwide because newly evolved pathogen strains have consistently overcome major resistance genes. The potato RB gene, derived from the wild species Solanum bulbocastanum, confers resistance to most P. infestans strains through recognition of members of the pathogen effector family IPI-O. While the majority of IPI-O proteins are recognized by RB to elicit resistance (e.g. IPI-O1, IPI-O2), some family members are able to elude detection (e.g. IPI-O4). In addition, IPI-O4 blocks recognition of IPI-O1, leading to inactivation of RB-mediated programmed cell death. Here, we report results that elucidate molecular mechanisms governing resistance elicitation or suppression of RB by IPI-O. Our data indicate self-association of the RB coiled coil (CC) domain as well as a physical interaction between this domain and the effectors IPI-O4 and IPI-O1. We identified four amino acids within IPI-O that are critical for interaction with the RB CC domain and one of these amino acids, at position 129, determines hypersensitive response (HR) elicitation in planta. IPI-O1 mutant L129P fails to induce HR in presence of RB while IPI-O4 P129L gains the ability to induce an HR. Like IPI-O4, IPI-O1 L129P is also able to suppress the HR mediated by RB, indicating a critical step in the evolution of this gene family. Our results point to a model in which IPI-O effectors can affect RB function through interaction with the RB CC domain.
DOI: 10.1371/journal.ppat.1002595
PubMed: 22438813
PubMed Central: PMC3305431
Affiliations:
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The potato RB gene, derived from the wild species Solanum bulbocastanum, confers resistance to most P. infestans strains through recognition of members of the pathogen effector family IPI-O. While the majority of IPI-O proteins are recognized by RB to elicit resistance (e.g. IPI-O1, IPI-O2), some family members are able to elude detection (e.g. IPI-O4). In addition, IPI-O4 blocks recognition of IPI-O1, leading to inactivation of RB-mediated programmed cell death. Here, we report results that elucidate molecular mechanisms governing resistance elicitation or suppression of RB by IPI-O. Our data indicate self-association of the RB coiled coil (CC) domain as well as a physical interaction between this domain and the effectors IPI-O4 and IPI-O1. We identified four amino acids within IPI-O that are critical for interaction with the RB CC domain and one of these amino acids, at position 129, determines hypersensitive response (HR) elicitation in planta. IPI-O1 mutant L129P fails to induce HR in presence of RB while IPI-O4 P129L gains the ability to induce an HR. Like IPI-O4, IPI-O1 L129P is also able to suppress the HR mediated by RB, indicating a critical step in the evolution of this gene family. Our results point to a model in which IPI-O effectors can affect RB function through interaction with the RB CC domain.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22438813</PMID><DateCompleted><Year>2012</Year><Month>07</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1553-7374</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>3</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PLoS pathogens</Title><ISOAbbreviation>PLoS Pathog</ISOAbbreviation></Journal><ArticleTitle>Molecular determinants of resistance activation and suppression by Phytophthora infestans effector IPI-O.</ArticleTitle><Pagination><MedlinePgn>e1002595</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.ppat.1002595</ELocationID><Abstract><AbstractText>Despite intensive breeding efforts, potato late blight, caused by the oomycete pathogen Phytophthora infestans, remains a threat to potato production worldwide because newly evolved pathogen strains have consistently overcome major resistance genes. The potato RB gene, derived from the wild species Solanum bulbocastanum, confers resistance to most P. infestans strains through recognition of members of the pathogen effector family IPI-O. While the majority of IPI-O proteins are recognized by RB to elicit resistance (e.g. IPI-O1, IPI-O2), some family members are able to elude detection (e.g. IPI-O4). In addition, IPI-O4 blocks recognition of IPI-O1, leading to inactivation of RB-mediated programmed cell death. Here, we report results that elucidate molecular mechanisms governing resistance elicitation or suppression of RB by IPI-O. Our data indicate self-association of the RB coiled coil (CC) domain as well as a physical interaction between this domain and the effectors IPI-O4 and IPI-O1. We identified four amino acids within IPI-O that are critical for interaction with the RB CC domain and one of these amino acids, at position 129, determines hypersensitive response (HR) elicitation in planta. IPI-O1 mutant L129P fails to induce HR in presence of RB while IPI-O4 P129L gains the ability to induce an HR. Like IPI-O4, IPI-O1 L129P is also able to suppress the HR mediated by RB, indicating a critical step in the evolution of this gene family. Our results point to a model in which IPI-O effectors can affect RB function through interaction with the RB CC domain.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Plant Pathology, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Zhenyu</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Halterman</LastName><ForeName>Dennis A</ForeName><Initials>DA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>03</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Pathog</MedlineTA><NlmUniqueID>101238921</NlmUniqueID><ISSNLinking>1553-7366</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>PLoS Pathog. 2012 Sep;8(9). doi:10.1371/annotation/75775518-f06e-4148-a639-31cfc6972b2e</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D060467" MajorTopicYN="N">Disease Resistance</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017343" MajorTopicYN="N">Genes, 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IdType="pubmed">21278123</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Wisconsin</li></region></list><tree><noCountry><name sortKey="Halterman, Dennis A" sort="Halterman, Dennis A" uniqKey="Halterman D" first="Dennis A" last="Halterman">Dennis A. Halterman</name><name sortKey="Liu, Zhenyu" sort="Liu, Zhenyu" uniqKey="Liu Z" first="Zhenyu" last="Liu">Zhenyu Liu</name></noCountry><country name="États-Unis"><region name="Wisconsin"><name sortKey="Chen, Yu" sort="Chen, Yu" uniqKey="Chen Y" first="Yu" last="Chen">Yu Chen</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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