Reshaping the Primary Cell Wall: Dual Effects on Plant Resistance to and Heat Stress Response.

Temperature elevation drastically affects plant defense responses to and inhibits the major source of resistance in , 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 gene as a major gene involved in plant response to  at both 27°C and an elevated temperature, 30°C. We functionally validated  as a susceptibility gene involved in resistance to  at both 27 and 30°C through a reverse genetic approach. We provide evidence that the  mutant 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, the  mutant still showed enhanced resistance to  with delayed onset of bacterial wilt symptoms. We demonstrated that the mutant had constitutive expression of the defense-related gene , 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 resistance to , remaining effective under heat stress. We expect that these results will help to identify robust genetic sources of resistance to  in 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.