BrHDA6 mediates nonhistone deacetylation of BrSOT12 to positively regulate downy mildew resistance in .

Downy mildew is a major disease that significantly impacts the yield and quality of . While histone deacetylase ( family members are implicated in stress responses, their role in regulating downy mildew resistance in remains unclear. Herein, we treated the susceptible line R32 with Trichostatin A (TSA), a potent inhibitor. Notably, TSA application significantly enhanced the susceptibility of seedlings to downy mildew infection, demonstrating that plays a crucial role in mediating resistance against this pathogen. Subsequently, we conducted phylogenetic analysis of family members and performed high-throughput sequencing to assess gene expression patterns in the resistant (R31) and susceptible (R32) lines following downy mildew inoculation. Notably, the expression of was significantly higher in the resistant line R31 compared to the susceptible line R32, suggesting its potential role in disease resistance. Using a genetic transformation system, we generated stable transgenic plants overexpressing or silenced for . Inoculation with the downy mildew pathogen revealed that positively regulates disease resistance. Modification omics and parallel reaction monitoring analysis demonstrated that BrHDA6 directly reduces the acetylation level of sulphotransferase 12 (BrSOT12), which likely enhances sulfotransferase activity, consequently boosting salicylic acid production during downy mildew infection. Interaction between BrHDA6 and BrSOT12 was further validated through yeast two-hybrid and dual-luciferase assays. Our study reveals that confers downy mildew resistance in through nonhistone protein deacetylation of BrSOT12, uncovering a novel regulatory mechanism in plant-pathogen interactions.