Quantitative and qualitative stem rust resistance factors in barley are associated with transcriptional suppression of defense regulons.
Identifieur interne : 000741 ( Main/Exploration ); précédent : 000740; suivant : 000742Quantitative and qualitative stem rust resistance factors in barley are associated with transcriptional suppression of defense regulons.
Auteurs : Matthew J. Moscou [États-Unis] ; Nick Lauter ; Brian Steffenson ; Roger P. WiseSource :
- PLoS genetics [ 1553-7404 ] ; 2011.
Descripteurs français
- KwdFr :
- Allèles (MeSH), Basidiomycota (génétique), Gènes de plante (MeSH), Hordeum (génétique), Hordeum (immunologie), Hordeum (microbiologie), Immunité des plantes (génétique), Interactions hôte-pathogène (MeSH), Locus de caractère quantitatif (génétique), Phénotype (MeSH), Plant (génétique), Plant (immunologie), Régulation de l'expression des gènes végétaux (immunologie), Tiges de plante (génétique), Tiges de plante (immunologie), Tiges de plante (microbiologie), Transcription génétique (MeSH).
- MESH :
- génétique : Basidiomycota, Hordeum, Immunité des plantes, Locus de caractère quantitatif, Plant, Tiges de plante.
- immunologie : Hordeum, Plant, Régulation de l'expression des gènes végétaux, Tiges de plante.
- microbiologie : Hordeum, Tiges de plante.
- Allèles, Gènes de plante, Interactions hôte-pathogène, Phénotype, Transcription génétique.
English descriptors
- KwdEn :
- Alleles (MeSH), Basidiomycota (genetics), Gene Expression Regulation, Plant (immunology), Genes, Plant (MeSH), Hordeum (genetics), Hordeum (immunology), Hordeum (microbiology), Host-Pathogen Interactions (MeSH), Phenotype (MeSH), Plant Immunity (genetics), Plant Stems (genetics), Plant Stems (immunology), Plant Stems (microbiology), Quantitative Trait Loci (genetics), Seedlings (genetics), Seedlings (immunology), Transcription, Genetic (MeSH).
- MESH :
- genetics : Basidiomycota, Hordeum, Plant Immunity, Plant Stems, Quantitative Trait Loci, Seedlings.
- immunology : Gene Expression Regulation, Plant, Hordeum, Plant Stems, Seedlings.
- microbiology : Hordeum, Plant Stems.
- Alleles, Genes, Plant, Host-Pathogen Interactions, Phenotype, Transcription, Genetic.
Abstract
Stem rust (Puccinia graminis f. sp. tritici; Pgt) is a devastating fungal disease of wheat and barley. Pgt race TTKSK (isolate Ug99) is a serious threat to these Triticeae grain crops because resistance is rare. In barley, the complex Rpg-TTKSK locus on chromosome 5H is presently the only known source of qualitative resistance to this aggressive Pgt race. Segregation for resistance observed on seedlings of the Q21861 × SM89010 (QSM) doubled-haploid (DH) population was found to be predominantly qualitative, with little of the remaining variance explained by loci other than Rpg-TTKSK. In contrast, analysis of adult QSM DH plants infected by field inoculum of Pgt race TTKSK in Njoro, Kenya, revealed several additional quantitative trait loci that contribute to resistance. To molecularly characterize these loci, Barley1 GeneChips were used to measure the expression of 22,792 genes in the QSM population after inoculation with Pgt race TTKSK or mock-inoculation. Comparison of expression Quantitative Trait Loci (eQTL) between treatments revealed an inoculation-dependent expression polymorphism implicating Actin depolymerizing factor3 (within the Rpg-TTKSK locus) as a candidate susceptibility gene. In parallel, we identified a chromosome 2H trans-eQTL hotspot that co-segregates with an enhancer of Rpg-TTKSK-mediated, adult plant resistance discovered through the Njoro field trials. Our genome-wide eQTL studies demonstrate that transcript accumulation of 25% of barley genes is altered following challenge by Pgt race TTKSK, but that few of these genes are regulated by the qualitative Rpg-TTKSK on chromosome 5H. It is instead the chromosome 2H trans-eQTL hotspot that orchestrates the largest inoculation-specific responses, where enhanced resistance is associated with transcriptional suppression of hundreds of genes scattered throughout the genome. Hence, the present study associates the early suppression of genes expressed in this host-pathogen interaction with enhancement of R-gene mediated resistance.
DOI: 10.1371/journal.pgen.1002208
PubMed: 21829384
PubMed Central: PMC3145622
Affiliations:
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Pgt race TTKSK (isolate Ug99) is a serious threat to these Triticeae grain crops because resistance is rare. In barley, the complex Rpg-TTKSK locus on chromosome 5H is presently the only known source of qualitative resistance to this aggressive Pgt race. Segregation for resistance observed on seedlings of the Q21861 × SM89010 (QSM) doubled-haploid (DH) population was found to be predominantly qualitative, with little of the remaining variance explained by loci other than Rpg-TTKSK. In contrast, analysis of adult QSM DH plants infected by field inoculum of Pgt race TTKSK in Njoro, Kenya, revealed several additional quantitative trait loci that contribute to resistance. To molecularly characterize these loci, Barley1 GeneChips were used to measure the expression of 22,792 genes in the QSM population after inoculation with Pgt race TTKSK or mock-inoculation. Comparison of expression Quantitative Trait Loci (eQTL) between treatments revealed an inoculation-dependent expression polymorphism implicating Actin depolymerizing factor3 (within the Rpg-TTKSK locus) as a candidate susceptibility gene. In parallel, we identified a chromosome 2H trans-eQTL hotspot that co-segregates with an enhancer of Rpg-TTKSK-mediated, adult plant resistance discovered through the Njoro field trials. Our genome-wide eQTL studies demonstrate that transcript accumulation of 25% of barley genes is altered following challenge by Pgt race TTKSK, but that few of these genes are regulated by the qualitative Rpg-TTKSK on chromosome 5H. It is instead the chromosome 2H trans-eQTL hotspot that orchestrates the largest inoculation-specific responses, where enhanced resistance is associated with transcriptional suppression of hundreds of genes scattered throughout the genome. Hence, the present study associates the early suppression of genes expressed in this host-pathogen interaction with enhancement of R-gene mediated resistance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21829384</PMID><DateCompleted><Year>2011</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>7</Issue><PubDate><Year>2011</Year><Month>Jul</Month></PubDate></JournalIssue><Title>PLoS genetics</Title><ISOAbbreviation>PLoS Genet</ISOAbbreviation></Journal><ArticleTitle>Quantitative and qualitative stem rust resistance factors in barley are associated with transcriptional suppression of defense regulons.</ArticleTitle><Pagination><MedlinePgn>e1002208</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1002208</ELocationID><Abstract><AbstractText>Stem rust (Puccinia graminis f. sp. tritici; Pgt) is a devastating fungal disease of wheat and barley. Pgt race TTKSK (isolate Ug99) is a serious threat to these Triticeae grain crops because resistance is rare. In barley, the complex Rpg-TTKSK locus on chromosome 5H is presently the only known source of qualitative resistance to this aggressive Pgt race. Segregation for resistance observed on seedlings of the Q21861 × SM89010 (QSM) doubled-haploid (DH) population was found to be predominantly qualitative, with little of the remaining variance explained by loci other than Rpg-TTKSK. In contrast, analysis of adult QSM DH plants infected by field inoculum of Pgt race TTKSK in Njoro, Kenya, revealed several additional quantitative trait loci that contribute to resistance. To molecularly characterize these loci, Barley1 GeneChips were used to measure the expression of 22,792 genes in the QSM population after inoculation with Pgt race TTKSK or mock-inoculation. Comparison of expression Quantitative Trait Loci (eQTL) between treatments revealed an inoculation-dependent expression polymorphism implicating Actin depolymerizing factor3 (within the Rpg-TTKSK locus) as a candidate susceptibility gene. In parallel, we identified a chromosome 2H trans-eQTL hotspot that co-segregates with an enhancer of Rpg-TTKSK-mediated, adult plant resistance discovered through the Njoro field trials. Our genome-wide eQTL studies demonstrate that transcript accumulation of 25% of barley genes is altered following challenge by Pgt race TTKSK, but that few of these genes are regulated by the qualitative Rpg-TTKSK on chromosome 5H. It is instead the chromosome 2H trans-eQTL hotspot that orchestrates the largest inoculation-specific responses, where enhanced resistance is associated with transcriptional suppression of hundreds of genes scattered throughout the genome. Hence, the present study associates the early suppression of genes expressed in this host-pathogen interaction with enhancement of R-gene mediated resistance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moscou</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Bioinformatics and Computational Biology Graduate Program, Iowa State University, Ames, Iowa, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lauter</LastName><ForeName>Nick</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Steffenson</LastName><ForeName>Brian</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Wise</LastName><ForeName>Roger P</ForeName><Initials>RP</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>07</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Genet</MedlineTA><NlmUniqueID>101239074</NlmUniqueID><ISSNLinking>1553-7390</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000483" MajorTopicYN="N">Alleles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001487" MajorTopicYN="N">Basidiomycota</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017343" MajorTopicYN="N">Genes, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001467" MajorTopicYN="N">Hordeum</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057865" MajorTopicYN="N">Plant Immunity</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018547" MajorTopicYN="N">Plant Stems</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D040641" MajorTopicYN="N">Quantitative Trait Loci</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D036226" MajorTopicYN="N">Seedlings</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>11</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>06</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>8</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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IdType="pubmed">15807783</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Iowa</li></region><settlement><li>Ames (Iowa)</li></settlement><orgName><li>Université d'État de l'Iowa</li></orgName></list><tree><noCountry><name sortKey="Lauter, Nick" sort="Lauter, Nick" uniqKey="Lauter N" first="Nick" last="Lauter">Nick Lauter</name><name sortKey="Steffenson, Brian" sort="Steffenson, Brian" uniqKey="Steffenson B" first="Brian" last="Steffenson">Brian Steffenson</name><name sortKey="Wise, Roger P" sort="Wise, Roger P" uniqKey="Wise R" first="Roger P" last="Wise">Roger P. Wise</name></noCountry><country name="États-Unis"><region name="Iowa"><name sortKey="Moscou, Matthew J" sort="Moscou, Matthew J" uniqKey="Moscou M" first="Matthew J" last="Moscou">Matthew J. Moscou</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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