An atypical NLR gene confers bacterial wilt susceptibility in Arabidopsis.
Arabidopsis thaliana
GWAS
R gene
Ralstonia solanacearum
susceptibility
type III effectors
Journal
Plant communications
ISSN: 2590-3462
Titre abrégé: Plant Commun
Pays: China
ID NLM: 101769147
Informations de publication
Date de publication:
11 09 2023
11 09 2023
Historique:
received:
29
07
2022
revised:
19
01
2023
accepted:
20
04
2023
medline:
14
9
2023
pubmed:
26
4
2023
entrez:
26
4
2023
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 37098653
pii: S2590-3462(23)00118-9
doi: 10.1016/j.xplc.2023.100607
pmc: PMC10504594
pii:
doi:
Substances chimiques
Bacterial Proteins
0
SGT1 protein, Arabidopsis
EC 2.4.1.-
Glucosyltransferases
EC 2.4.1.-
Arabidopsis Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
100607Informations de copyright
Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.
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