Pepper mildew resistance locus O 1 (MLO1) context-specifically induces high-temperature-specific immunity and thermotolerance.

Plant diseases tend to be more serious under high-temperature/high-humidity (HTHH) conditions than at room temperature; thus, disease resistance under HTHH is a bottleneck for plant survival. However, how plants cope with diseases under HTHH remains poorly understood. Herein, using the pathosystem consisting of pepper and R. solanacearum as an example and expression profiling, loss- and gain-of-function assays involving virus-induced gene silencing and overexpression in pepper plants, and protein-protein interaction assays, the functions of CaMLO1 and CaPUB21 in pepper immunity against R. solanacearum at 28°C or 37°C (with 80% humidity) were comparatively characterized. The results showed that CaMLO1 acted negatively in pepper immunity against R. solanacearum at 28°C but positively at 37°C. In contrast, CaPUB21 acted positively upon R. solanacearum at 28°C but negatively at 37°C. Importantly, CaPUB21 interacted with CaMLO1 under all of the tested conditions, but only the CaPUB21-CaMLO1 interaction in response to R. solanacearum at 37°C or exposure to 37°C led to CaMLO1 degradation, thereby turning off inappropriate defence responses against R. solanacearum at 37°C and high-temperature stress. The results highlight that CaMLO1 and CaPUB21 function distinctly in pepper immunity against R. solanacearum in an environment-dependent manner and interact with each other, leading to the degradation of CaMLO1 specifically in response to R. solanacearum at 37°C or exposure to high temperature stress to turn off the inappropriate defence response mediated by CaMLO1.