Flax rust resistance gene specificity is based on direct resistance-avirulence protein interactions.
Identifieur interne : 000156 ( Main/Corpus ); précédent : 000155; suivant : 000157Flax rust resistance gene specificity is based on direct resistance-avirulence protein interactions.
Auteurs : Jeffrey G. Ellis ; Peter N. Dodds ; Gregory J. LawrenceSource :
- Annual review of phytopathology [ 0066-4286 ] ; 2007.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Plant Proteins.
- genetics : Flax, Immunity, Innate, Plant Diseases.
- immunology : Flax, Plant Diseases, Plant Proteins.
- Necrosis, Virulence.
Abstract
Genetic studies of the flax-flax rust interaction led to the formulation of the gene-for-gene hypothesis and identified resistance genes (R) in the host plant and pathogenicity genes, including avirulence (Avr) and inhibitor of avirulence genes (I), in the rust pathogen. R genes have now been cloned from four of the five loci in flax and all encode proteins of the Toll, Interleukin-1 receptor, R gene-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) class. Avr genes have been cloned from four loci in flax rust and encode small secreted proteins with no between locus similarity and no close homologs in current data bases. It is postulated that Avr proteins enter the host cell, have virulence effector functions, and in resistant host genotypes, are recognized by direct and specific interaction with host R proteins, leading to activation of rust resistance defense responses. Direct interaction between R and Avr proteins is the basis of gene-for-gene specificity in the flax-flax rust system and both R and Avr genes have the signatures of diversifying selection, suggesting the existence of a coevolutionary arms race between the host plant and its obligate rust pathogen.
DOI: 10.1146/annurev.phyto.45.062806.094331
PubMed: 17430087
Links to Exploration step
pubmed:17430087Le document en format XML
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<author><name sortKey="Ellis, Jeffrey G" sort="Ellis, Jeffrey G" uniqKey="Ellis J" first="Jeffrey G" last="Ellis">Jeffrey G. Ellis</name>
<affiliation><nlm:affiliation>CSIRO-Plant Industry, GPO Box 1600, Canberra ACT 2601, Australia. jeff.ellis@csiro.au</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Dodds, Peter N" sort="Dodds, Peter N" uniqKey="Dodds P" first="Peter N" last="Dodds">Peter N. Dodds</name>
</author>
<author><name sortKey="Lawrence, Gregory J" sort="Lawrence, Gregory J" uniqKey="Lawrence G" first="Gregory J" last="Lawrence">Gregory J. Lawrence</name>
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<author><name sortKey="Ellis, Jeffrey G" sort="Ellis, Jeffrey G" uniqKey="Ellis J" first="Jeffrey G" last="Ellis">Jeffrey G. Ellis</name>
<affiliation><nlm:affiliation>CSIRO-Plant Industry, GPO Box 1600, Canberra ACT 2601, Australia. jeff.ellis@csiro.au</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Dodds, Peter N" sort="Dodds, Peter N" uniqKey="Dodds P" first="Peter N" last="Dodds">Peter N. Dodds</name>
</author>
<author><name sortKey="Lawrence, Gregory J" sort="Lawrence, Gregory J" uniqKey="Lawrence G" first="Gregory J" last="Lawrence">Gregory J. Lawrence</name>
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<series><title level="j">Annual review of phytopathology</title>
<idno type="ISSN">0066-4286</idno>
<imprint><date when="2007" type="published">2007</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Flax (genetics)</term>
<term>Flax (immunology)</term>
<term>Immunity, Innate (genetics)</term>
<term>Necrosis (MeSH)</term>
<term>Plant Diseases (genetics)</term>
<term>Plant Diseases (immunology)</term>
<term>Plant Proteins (genetics)</term>
<term>Plant Proteins (immunology)</term>
<term>Virulence (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Flax</term>
<term>Immunity, Innate</term>
<term>Plant Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Flax</term>
<term>Plant Diseases</term>
<term>Plant Proteins</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Necrosis</term>
<term>Virulence</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Genetic studies of the flax-flax rust interaction led to the formulation of the gene-for-gene hypothesis and identified resistance genes (R) in the host plant and pathogenicity genes, including avirulence (Avr) and inhibitor of avirulence genes (I), in the rust pathogen. R genes have now been cloned from four of the five loci in flax and all encode proteins of the Toll, Interleukin-1 receptor, R gene-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) class. Avr genes have been cloned from four loci in flax rust and encode small secreted proteins with no between locus similarity and no close homologs in current data bases. It is postulated that Avr proteins enter the host cell, have virulence effector functions, and in resistant host genotypes, are recognized by direct and specific interaction with host R proteins, leading to activation of rust resistance defense responses. Direct interaction between R and Avr proteins is the basis of gene-for-gene specificity in the flax-flax rust system and both R and Avr genes have the signatures of diversifying selection, suggesting the existence of a coevolutionary arms race between the host plant and its obligate rust pathogen.</div>
</front>
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<DateCompleted><Year>2007</Year>
<Month>10</Month>
<Day>12</Day>
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<DateRevised><Year>2008</Year>
<Month>11</Month>
<Day>21</Day>
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<JournalIssue CitedMedium="Print"><Volume>45</Volume>
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<Title>Annual review of phytopathology</Title>
<ISOAbbreviation>Annu Rev Phytopathol</ISOAbbreviation>
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<ArticleTitle>Flax rust resistance gene specificity is based on direct resistance-avirulence protein interactions.</ArticleTitle>
<Pagination><MedlinePgn>289-306</MedlinePgn>
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<Abstract><AbstractText>Genetic studies of the flax-flax rust interaction led to the formulation of the gene-for-gene hypothesis and identified resistance genes (R) in the host plant and pathogenicity genes, including avirulence (Avr) and inhibitor of avirulence genes (I), in the rust pathogen. R genes have now been cloned from four of the five loci in flax and all encode proteins of the Toll, Interleukin-1 receptor, R gene-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) class. Avr genes have been cloned from four loci in flax rust and encode small secreted proteins with no between locus similarity and no close homologs in current data bases. It is postulated that Avr proteins enter the host cell, have virulence effector functions, and in resistant host genotypes, are recognized by direct and specific interaction with host R proteins, leading to activation of rust resistance defense responses. Direct interaction between R and Avr proteins is the basis of gene-for-gene specificity in the flax-flax rust system and both R and Avr genes have the signatures of diversifying selection, suggesting the existence of a coevolutionary arms race between the host plant and its obligate rust pathogen.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ellis</LastName>
<ForeName>Jeffrey G</ForeName>
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<Author ValidYN="Y"><LastName>Dodds</LastName>
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<Author ValidYN="Y"><LastName>Lawrence</LastName>
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<Language>eng</Language>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D019597" MajorTopicYN="N">Flax</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D009336" MajorTopicYN="N">Necrosis</DescriptorName>
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<MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName>
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<NumberOfReferences>33</NumberOfReferences>
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