ArticlePlant communications2023
An atypical NLR gene confers bacterial wilt susceptibility in Arabidopsis.
Article in Plant communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Pathogenicity and virulence ofVirulence · 2026Review
- New biologically relevant resistance to bacterial wilt in heat-stressed tomato revealed by two-reference Genome Wide Association.PLoS genetics · 2026Article
- Transition metal-enhanced immunity in Arabidopsis roots via an NLR pair.Nature plants · 2026Article
- Overexpression of a novel CC-NBS-LRR gene NtRPP13 confers enhanced resistance to Ralstonia solanacearum in tobacco.Plant cell reports · 2025Article
- Molecular Dialog ofInternational journal of molecular sciences · 2025Review
- The receptor MIK2 interacts with the kinase RKS1 to control quantitative disease resistance to Xanthomonas campestris.Plant physiology · 2024Article
- Toward Ecologically Relevant Genetics of Interactions Between Host Plants and Plant Growth-Promoting Bacteria.Advanced genetics (Hoboken, N.J.) · 2024Article
- A pan-genome of 69 Arabidopsis thaliana accessions reveals a conserved genome structure throughout the global species range.Nature genetics · 2024Article
- Genetic architecture of the response ofFrontiers in plant science · 2023Article
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Authors and funding
14 authors.
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No grant is acknowledged in the PubMed record.
Abstract
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.
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