Arabidopsis spliceosome factor SmD3-b modulates immunity to Pseudomonas syringae infection

SmD3 is a core protein of small nuclear ribonucleoproteins essential for pre-mRNA splicing. To assess the role of Arabidopsis SmD3-b in response to biotic stress we investigated sensitivity of the smd3-b mutant to Pseudomonas syringae pv. tomato DC3000 infection and its pathogenesis effectors flg22, elf18 and coronatine. We show that the mutant exhibits enhanced susceptibility to Pst accompanied with marked changes in the expression of key pathogenesis markers. mRNA levels of major biotic stress response factors were also altered upon treatment with Pseudomonas effectors. Our genome-wide transcriptome analysis of smd3-b mutant infected with Pst confirmed that lack of SmD3 protein deregulates defense to Pst DC3000 infection on the transcriptional level, including defects in splicing and altered pattern of alternative splicing. In addition, callose deposition, which is another marker of plant immunity, was strongly induced by elf18 and flg22 in the mutant, whereas production of reactive oxygen species triggered by flg22 was reduced. Finally, detection of phosphorylated forms of MPK3, MPK6 and MPK4/11 revealed higher activation of all MAPKs in the smd3-b mutant. All our data indicate that SmD3 contributes to plant immune response possibly via regulation of mRNA splicing of the key pathogenesis factors. Transcriptome profiles of Col-0 and smd3-b mutant plants after pathogen or control treatment using RNA-seq (three biological replicates).