Temperature elevation drastically affects plant defense responses to Ralstonia solanacearum and inhibits the major source of resistance in Arabidopsis thaliana, 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 to R. solanacearum at both 27°C and elevated temperature, 30°C. We functionally validated CESA3 as a susceptibility gene involved in resistance to R. solanacearum at both 27°C and 30°C through a reverse genetic approach. We provide evidence that the cesa3 mre1 mutant enhances resistance to bacterial disease and that resistance is associated with an alteration of root cell morphology conserved at elevated temperature. However, even by forcing the entry of the bacterium to bypass the primary cell wall barrier, the cesa3 mre1 mutant still showed enhanced resistance to R. solanacearum with delayed onset of bacterial wilt symptoms. We demonstrated that the cesa3 mre1 mutant had constitutive expression of the defense-related gene VSP1 which is up-regulated at elevated temperature 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 R. solanacearum, remaining effective under heat stress. We expect that these results will help to identify robust genetic sources of resistance to R. solanacearum in the context of global warming.