Sheng Yang

It has previously been found that CaWRKY40 is employed by pepper to activate immunity against Ralstonia solanacearum and to activate thermotolerance context-specifically, but the underlying mechanisms are not fully understood. Here, CaGβ, a subunit in the heterotrimeric G protein complex that was originally found to probably interact with CaWRKY40, was expressional and functionally characterized; the results showed that CaGβ was upregulated by R. solanacearum infection; its silencing by virus-induced silencing impaired pepper immunity against R. solanacearum infection, accompanied by downregulation of immunity-related marker genes, including CaPR1, CaDEF1, CaNPR1, and CaPR-STH2. In addition, CaGβ–CaWRKY40 interaction was confirmed by BiFC and pull-down assay using prokaryotically expressed proteins, and activations of immunity-related CaPR1, CaPR-STH2, and CaNPR1 by CaWRKY40 were all promoted, but the activation of thermotolerance-related CaHSP24 by CaWRKY40 blocked CaGβ through its interaction with CaWRKY40. All these data indicate that immunity against R. solanacearum and its antagonism to thermotolerance in pathogen-infected pepper plants are mediated by CaWRKY40 through physical interaction with CaGβ.

Pepper (Capsicum annuum), a widely cultivated vegetable of significant economic importance globally, is frequently subjected to attacks from pathogens such as Ralstonia solanacearum, as well as high-temperature stress. However, the mechanisms by which pepper combats these stresses remain poorly understood. Herein, we reported that the expression of the leucine-rich repeat protein CaLRR13, which lacks a nucleotide-binding site (NBS), kinase domains, and a transmembrane region, was transcriptionally activated by both R. solanacearum inoculation and high-temperature stress. Through transient overexpression in the epidermal cells of Nicotiana benthamiana leaves, we found that CaLRR13 localized in both the cytoplasm and the nuclei. Reducing the expression of CaLRR13 via virus-induced gene silencing (VIGS) increased the sensitivity of pepper to R. solanacearum infection and high-temperature exposure, accompanied by reduced expression of immunity- and thermotolerance-related genes, including CaWRKY40, CaPR1, CaNPR1, CaDEF1, and CaHSP24. In contrast, transient overexpression of CaLRR13 in pepper leaves induced a like-hypersensitive response (HR) and enhanced the expression of the aforementioned immunity- and thermotolerance-related genes. Thus, we conclude that CaLRR13 plays a positive role in pepper immunity against R. solanacearum and thermotolerance, providing a new perspective on the crosstalk and management of plant responses to these two stresses.