Arabidopsisspliceosome factor SmD3 modulates immunity toPseudomonas syringaeinfection

AbstractSmD3 is a core component of the small nuclear ribonucleoprotein (snRNP) that is essential for pre-mRNA splicing. The role ofArabidopsisSmD3 in plant immunity was assessed by testing sensitivity ofsmd3aandsmd3bmutants toPseudomonas syringaepv.tomato(Pst) DC3000 infection and its pathogenesis effectors flagellin (flg22), EF-Tu (elf18) and coronatine (COR). Bothsmd3mutants exhibited enhanced susceptibility toPstaccompanied by marked changes in the expression of key pathogenesis markers. mRNA levels of these factors were also altered upon treatment withPseudomonaseffectors. We showed that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. Our genome-wide transcriptome analysis of thesmd3b-1mutant infected withPstrevealed that lack of SmD3-b deregulates defense againstPstinfection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. Other changes in thesmd3b-1mutant involved enhanced elf18- and flg22-induced callose deposition, reduction of flg22-triggered production of early ROS and boost of secondary ROS caused byPstinfection. Together, our data indicate that SmD3 contributes to the plant immune response possibly via regulation of mRNA splicing of key pathogenesis factors.