Abstract
Temperature elevation drastically affects plant defense responses to Ralstonia solanacearum and inhibits the major source of resistance in Arabidopsis thaliana, which is mediated by the receptor pair RRS1-R/RPS4. In this study, we refined a previous genome-wide association (GWA) mapping analysis by using a local score approach and detected the primary cell wall CESA3 gene as a major gene involved in plant response toR. solanacearumat both 27°C and an elevated temperature, 30°C. We functionally validatedCESA3as a susceptibility gene involved in resistance toR. solanacearumat both 27 and 30°C through a reverse genetic approach. We provide evidence that thecesa3mre1mutant enhances resistance to bacterial disease and that resistance is associated with an alteration of root cell morphology conserved at elevated temperatures. However, even by forcing the entry of the bacterium to bypass the primary cell wall barrier, thecesa3mre1mutant still showed enhanced resistance toR. solanacearumwith delayed onset of bacterial wilt symptoms. We demonstrated that thecesa3mre1mutant had constitutive expression of the defense-related geneVSP1, which is upregulated at elevated temperatures, and that during infection, its expression level is maintained higher than in the wild-type Col-0. In conclusion, this study reveals that alteration of the primary cell wall by mutating the cellulose synthase subunit CESA3 contributes to enhanced resistanceto R. solanacearum,remaining effective under heat stress. We expect that these results will help to identify robust genetic sources of resistance toR. solanacearumin the context of global warming. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
Published Version
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