Long-chain base kinase1 promotes salicylic acid-mediated stomatal immunity in Arabidopsis thaliana

Stomatal closure is an inducible form of defense that plants exert upon activation of pattern-triggered immunity (PTI). Arabidopsis long-chain base kinase 1 (LCBK1) phosphorylates phytosphingosine, which is essential for PTI-induced stomatal closure. Impairment of stomatal closure of lcbk1 mutants can be rescued by exogenous application of phosphorylated phytosphingosine. PTI-induced stomatal closure also requires salicylic acid (SA). However, the role of LCBK1 in SA-mediated stomatal closure was not known. Here, we have shown that lcbk1 mutants are defective in pathogen-induced SA accumulation and show a reduced level of expression of SA biosynthesis genes such as ICS1 , PAD4 , and APD1 . Interestingly, the exogenous application of SA does not entirely restore the loss of immunity against pathogens in lcbk1 mutants. The lcbk1 mutants are also partially defective in SA-mediated stomatal closure. Application of phytosphingosine-phosphate activate stomatal closure in WT but not in SA biosynthetic mutant sid2 . LCBK1 interacts with polycomb-group repressor complex 2 protein MEDEA, which functions as an attenuator of SA-mediated defense. However, MEDEA is not involved in SA-mediated stomatal closure. Results altogether suggest that LCBK1 functions at the upstream of SA biosynthesis as well as at the downstream for SA-mediated stomatal immunity.