Quantitative disease resistance(QDR)remains the most prevalent form of plant resistance in crop fields and wild habitats.Genome-wide association studies(GWAS)have proved to be successful in deciphering the quantitativ...Quantitative disease resistance(QDR)remains the most prevalent form of plant resistance in crop fields and wild habitats.Genome-wide association studies(GWAS)have proved to be successful in deciphering the quantitative genetic basis of complex traits such as QDR.To unravel the genetics of QDR to the devastating worldwide bacterial pathogen Ralstonia solanacearum,we performed a GWAS by challenging a highly polymorphic local mapping population of Arabidopsis thaliana with four R.solanacearum type III effector(T3E)mutants,identified as key pathogenicity determinants after a first screen on an A.thaliana core collection of 25 accessions.Although most quantitative trait loci(QTLs)were highly specific to the identity of the T3E mutant(ripAC,ripAG,ripAQ,and ripU),we finely mapped a common QTL located on a cluster of nucleotide-binding domain and leucine-rich repeat(NLR)genes that exhibited structural variation.We functionally validated one of these NLRs as a susceptibility factor in response to R.solanacearum,named it Bacterial Wilt Susceptibility 1(BWS1),and cloned two alleles that conferred contrasting levels of QDR.Further characterization indicated that expression of BWS1 leads to suppression of immunity triggered by different R.solanacearum effectors.In addition,we showed a direct interaction between BWS1 and RipAC T3E,and BWS1 and SUPPRESSOR OF G2 ALLELE OF skp1(SGT1b),the latter interaction being suppressed by RipAC.Together,our results highlight a putative role for BWS1 as a quantitative susceptibility factor directly targeted by the T3E RipAC,mediating negative regulation of the SGT1-dependent immune response.展开更多
基金supported by the Laboratoire d’Excellence(LABEX)TULIP(ANR-10-LABX-41)funded by a grant from the Lebanese University+4 种基金INRAE,Campus France,and the INRAE Plant Health and Environment division(SPE)for their support and fundinga PhD grant co-financed by the Occitanie Regional Council and the INRAE Plant Health and Environment division(SPE)funded by a grant from the French Ministry of National Education and Researchsupported by France Genomique National infrastructurefunded as part of the Investissement d’avenir program managed by Agence Nationale de la Recherche(contract ANR-10-INBS-09).
文摘Quantitative disease resistance(QDR)remains the most prevalent form of plant resistance in crop fields and wild habitats.Genome-wide association studies(GWAS)have proved to be successful in deciphering the quantitative genetic basis of complex traits such as QDR.To unravel the genetics of QDR to the devastating worldwide bacterial pathogen Ralstonia solanacearum,we performed a GWAS by challenging a highly polymorphic local mapping population of Arabidopsis thaliana with four R.solanacearum type III effector(T3E)mutants,identified as key pathogenicity determinants after a first screen on an A.thaliana core collection of 25 accessions.Although most quantitative trait loci(QTLs)were highly specific to the identity of the T3E mutant(ripAC,ripAG,ripAQ,and ripU),we finely mapped a common QTL located on a cluster of nucleotide-binding domain and leucine-rich repeat(NLR)genes that exhibited structural variation.We functionally validated one of these NLRs as a susceptibility factor in response to R.solanacearum,named it Bacterial Wilt Susceptibility 1(BWS1),and cloned two alleles that conferred contrasting levels of QDR.Further characterization indicated that expression of BWS1 leads to suppression of immunity triggered by different R.solanacearum effectors.In addition,we showed a direct interaction between BWS1 and RipAC T3E,and BWS1 and SUPPRESSOR OF G2 ALLELE OF skp1(SGT1b),the latter interaction being suppressed by RipAC.Together,our results highlight a putative role for BWS1 as a quantitative susceptibility factor directly targeted by the T3E RipAC,mediating negative regulation of the SGT1-dependent immune response.
