Proteins with conserved SET domain play a critical role in plant immunity. However, the means of organization and functions of these proteins are unclear, particularly in non-model plants such as pepper (Capsicum annum L.). Herein, we functionally characterized CaASHH3, a member of class II (the ASH1 homologs H3K36) proteins in pepper immunity against Ralstonia solanacearum and Pseudomonas syringae pv tomato DC3000 (Pst DC3000). The CaASHH3 was localized in the nucleus, and its transcript levels were significantly enhanced by R. solanacearum inoculation (RSI) and exogenous application of salicylic acid (SA), methyl jasmonate (MeJA), ethephon (ETH), and abscisic acid (ABA). Knockdown of CaASHH3 by virus-induced gene silencing (VIGS) compromised peppers’ resistance to RSI. Furthermore, silencing of CaASHH3 impaired hypersensitive-response (HR)-like cell death response due to RSI and downregulated defense-associated marker genes, including CaPR1, CaNPR1, and CaABR1. The CaASHH3 protein was revealed to affect the promoters of CaNPR1, CaPR1, and CaHSP24. Transiently over-expression of CaASHH3 in pepper leaves elicited HR-like cell death and upregulated immunity-related marker genes. To further study the role of CaASHH3 in plant defense in vivo, CaASHH3 transgenic plants were generated in Arabidopsis. Overexpression of CaASHH3 in transgenic Arabidopsis thaliana enhanced innate immunity against Pst DC3000. Furthermore, CaASHH3 over-expressing transgenic A. thaliana plants exhibited upregulated transcriptional levels of immunity-associated marker genes, such as AtNPR1, AtPR1, and AtPR2. These results collectively confirm the role of CaASHH3 as a positive regulator of plant cell death and pepper immunity against bacterial pathogens, which is regulated by signaling synergistically mediated by SA, JA, ET, and ABA.
Bacterial wilt, a severe disease that affects over 250 plant species, is caused by Ralstonia solanacearum through vascular system blockade. Although both plant immunity and dehydration tolerance might contribute to disease resistance, whether and how they are related are still unclear. Herein, we provide evidence that immunity against R. solanacearum and dehydration tolerance are coupled and regulated by CaPti1-CaERF4 module. By expression profiling, virus-induced gene silencing in pepper and overexpression in Nicotiana benthamiana, both CaPti1 and CaERF4 were upregulated by R. solanacearum inoculation, dehydration stress and exogenously applied ABA. They in turn phenocopied with each other in promoting pepper resistance to bacterial wilt not only by activating HR cell death and SA-dependent CaPR1, but also by activating dehydration tolerance related CaOSM1 and CaOSR1, and stomata closure to reduce water loss in ABA signaling dependent manner. Yeast-two hybrid assay showed that CaERF4 interacts with CaPti1, which was confirmed by co-immunoprecipitation and pull-down assays. Chromatin immunoprecipitation and electrophoretic mobility shift assay showed that, upon R. solanacearum inoculation, CaPR1, CaOSM1 and CaOSR1 were directly targeted and positively regulated by CaERF4 via binding GCC-box or DRE-box, which was potentiated by CaPti1. In addition, our data indicate that CaPti1-CaERF4 complex might act downstream ABA signaling, since the exogenously applied ABA did not alter stomata aperture regulated by CaPti1-CaERF4 module. Importantly, CaPti1-CaERF4 module was found also acts positively in pepper growth and response to dehydration stress. Collectively, the results suggest that immunity and dehydration tolerance are coupled and positively regulated by CaPti1-CaERF4 in pepper plants to enhance resistance against R. solanacearum.SummaryPepper immunity and dehydration tolerance are coupled and regulated by the CaPti1-CaERF4 module partially in a way related to ABA signaling and stomata closure.
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