Abstract
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.
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