The chloroplast protein RPH1 plays a role in the immune response of Arabidopsis to Phytophthora brassicae.
Identifieur interne : 001B65 ( Main/Corpus ); précédent : 001B64; suivant : 001B66The chloroplast protein RPH1 plays a role in the immune response of Arabidopsis to Phytophthora brassicae.
Auteurs : Khaoula Belhaj ; Baiqing Lin ; Felix MauchSource :
- The Plant journal : for cell and molecular biology [ 1365-313X ] ; 2009.
English descriptors
- KwdEn :
- Amino Acid Sequence (MeSH), Arabidopsis (genetics), Arabidopsis (immunology), Arabidopsis (metabolism), Arabidopsis Proteins (genetics), Arabidopsis Proteins (metabolism), Cell Death (MeSH), Chloroplasts (genetics), Chloroplasts (metabolism), DNA, Plant (genetics), Gene Expression Regulation, Plant (MeSH), Gene Silencing (MeSH), Genetic Complementation Test (MeSH), Hydrogen Peroxide (MeSH), Molecular Sequence Data (MeSH), Mutagenesis, Insertional (MeSH), Oxidative Stress (MeSH), Phytophthora (growth & development), Plant Diseases (genetics), Plant Diseases (immunology), Sequence Alignment (MeSH), Sequence Analysis, DNA (MeSH), Solanum tuberosum (genetics), Solanum tuberosum (metabolism).
- MESH :
- chemical , genetics : Arabidopsis Proteins, DNA, Plant.
- genetics : Arabidopsis, Chloroplasts, Plant Diseases, Solanum tuberosum.
- growth & development : Phytophthora.
- immunology : Arabidopsis, Plant Diseases.
- metabolism : Arabidopsis, Arabidopsis Proteins, Chloroplasts, Solanum tuberosum.
- Amino Acid Sequence, Cell Death, Gene Expression Regulation, Plant, Gene Silencing, Genetic Complementation Test, Hydrogen Peroxide, Molecular Sequence Data, Mutagenesis, Insertional, Oxidative Stress, Sequence Alignment, Sequence Analysis, DNA.
Abstract
Plant immune responses to pathogens are often associated with enhanced production of reactive oxygen species (ROS), known as the oxidative burst, and with rapid hypersensitive host cell death (the hypersensitive response, HR) at sites of attempted infection. It is generally accepted that the oxidative burst acts as a promotive signal for HR, and that HR is highly correlated with efficient disease resistance. We have identified the Arabidopsis mutant rph1 (resistance to Phytophthora 1), which is susceptible to the oomycete pathogen Phytophthora brassicae despite rapid induction of HR. The susceptibility of rph1 was specific for P. brassicae and coincided with a reduced oxidative burst, a runaway cell-death response, and failure to properly activate the expression of defence-related genes. From these results, we conclude that, in the immune response to P. brassicae, (i) HR is not sufficient to stop the pathogen, (ii) HR initiation can occur in the absence of a major oxidative burst, (iii) the oxidative burst plays a role in limiting the spread of cell death, and (iv) RPH1 is a positive regulator of the P. brassicae-induced oxidative burst and enhanced expression of defence-related genes. Surprisingly, RPH1 encodes an evolutionary highly conserved chloroplast protein, indicating a function of this organelle in activation of a subset of immune reactions in response to P. brassicae. The disease resistance-related role of RPH1 was not limited to the Arabidopsis model system. Silencing of the potato homolog StRPH1 in a resistant potato cultivar caused susceptibility to the late blight pathogen Phytophthora infestans.
DOI: 10.1111/j.1365-313X.2008.03779.x
PubMed: 19170932
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pubmed:19170932Le document en format XML
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It is generally accepted that the oxidative burst acts as a promotive signal for HR, and that HR is highly correlated with efficient disease resistance. We have identified the Arabidopsis mutant rph1 (resistance to Phytophthora 1), which is susceptible to the oomycete pathogen Phytophthora brassicae despite rapid induction of HR. The susceptibility of rph1 was specific for P. brassicae and coincided with a reduced oxidative burst, a runaway cell-death response, and failure to properly activate the expression of defence-related genes. From these results, we conclude that, in the immune response to P. brassicae, (i) HR is not sufficient to stop the pathogen, (ii) HR initiation can occur in the absence of a major oxidative burst, (iii) the oxidative burst plays a role in limiting the spread of cell death, and (iv) RPH1 is a positive regulator of the P. brassicae-induced oxidative burst and enhanced expression of defence-related genes. Surprisingly, RPH1 encodes an evolutionary highly conserved chloroplast protein, indicating a function of this organelle in activation of a subset of immune reactions in response to P. brassicae. The disease resistance-related role of RPH1 was not limited to the Arabidopsis model system. Silencing of the potato homolog StRPH1 in a resistant potato cultivar caused susceptibility to the late blight pathogen Phytophthora infestans.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19170932</PMID><DateCompleted><Year>2009</Year><Month>05</Month><Day>28</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1365-313X</ISSN><JournalIssue CitedMedium="Internet"><Volume>58</Volume><Issue>2</Issue><PubDate><Year>2009</Year><Month>Apr</Month></PubDate></JournalIssue><Title>The Plant journal : for cell and molecular biology</Title><ISOAbbreviation>Plant J</ISOAbbreviation></Journal><ArticleTitle>The chloroplast protein RPH1 plays a role in the immune response of Arabidopsis to Phytophthora brassicae.</ArticleTitle><Pagination><MedlinePgn>287-98</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1365-313X.2008.03779.x</ELocationID><Abstract><AbstractText>Plant immune responses to pathogens are often associated with enhanced production of reactive oxygen species (ROS), known as the oxidative burst, and with rapid hypersensitive host cell death (the hypersensitive response, HR) at sites of attempted infection. It is generally accepted that the oxidative burst acts as a promotive signal for HR, and that HR is highly correlated with efficient disease resistance. We have identified the Arabidopsis mutant rph1 (resistance to Phytophthora 1), which is susceptible to the oomycete pathogen Phytophthora brassicae despite rapid induction of HR. The susceptibility of rph1 was specific for P. brassicae and coincided with a reduced oxidative burst, a runaway cell-death response, and failure to properly activate the expression of defence-related genes. From these results, we conclude that, in the immune response to P. brassicae, (i) HR is not sufficient to stop the pathogen, (ii) HR initiation can occur in the absence of a major oxidative burst, (iii) the oxidative burst plays a role in limiting the spread of cell death, and (iv) RPH1 is a positive regulator of the P. brassicae-induced oxidative burst and enhanced expression of defence-related genes. Surprisingly, RPH1 encodes an evolutionary highly conserved chloroplast protein, indicating a function of this organelle in activation of a subset of immune reactions in response to P. brassicae. The disease resistance-related role of RPH1 was not limited to the Arabidopsis model system. Silencing of the potato homolog StRPH1 in a resistant potato cultivar caused susceptibility to the late blight pathogen Phytophthora infestans.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Belhaj</LastName><ForeName>Khaoula</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Biology, University of Fribourg, Fribourg, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Baiqing</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Mauch</LastName><ForeName>Felix</ForeName><Initials>F</Initials></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>2008</Year><Month>12</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Plant J</MedlineTA><NlmUniqueID>9207397</NlmUniqueID><ISSNLinking>0960-7412</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029681">Arabidopsis Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018744">DNA, Plant</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017360" MajorTopicYN="N">Arabidopsis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029681" MajorTopicYN="N">Arabidopsis Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002736" MajorTopicYN="N">Chloroplasts</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018744" MajorTopicYN="N">DNA, Plant</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020868" MajorTopicYN="N">Gene Silencing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005816" MajorTopicYN="N">Genetic Complementation Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016254" MajorTopicYN="N">Mutagenesis, Insertional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010838" MajorTopicYN="N">Phytophthora</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016415" MajorTopicYN="N">Sequence Alignment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017422" MajorTopicYN="N">Sequence Analysis, DNA</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011198" MajorTopicYN="N">Solanum tuberosum</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>1</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>1</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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