Phosphorylation of CAX transporters controls Ca^(2+)homeostasi

Plants rely on a sophisticated innate immune system to recognize and defend against invading pathogens.The first line of plant innate immunity,called pattern-triggered immunity(PTI),is initiated upon detection of pathogen-associated molecular patterns(PAMPs)by plasma-membrane-localized pattern recognition receptors(PRRs)(Jones and Dangl,2006).

Phosphorylation of an ethylene response factor by MPK3/MPK6 mediates negative feedback regulation of pathogen-induced ethylene biosynthesis in Arabidopsis

Plants under pathogen attack produce high levels of the gaseous phytohormone ethylene to induce plant defense responses via the ethylene signaling pathway.The 1-aminocyclopropane-1-carboxylate synthase(ACS)is a critical rate-limiting enzyme of ethylene biosynthesis.Transcriptional and post-translational upregulation of ACS2 and ACS6 by the mitogen-activated protein kinases MPK3 and MPK6 are previously shown to be crucial for pathogen-induced ethylene biosynthesis in Arabidopsis.Here,we report that the fungal pathogen Botrytis cinerea-induced ethylene biosynthesis in Arabidopsis is under the negative feedback regulation by ethylene signaling pathway.The ethylene response factor ERF1 A is further found to act downstream of ethylene signaling to negatively regulate the B.cinerea-induced ethylene biosynthesis via indirectly suppressing the expression of ACS2 and ACS6.Interestingly,ERF1 A is shown to also upregulate defensin genes directly and therefore promote Arabidopsis resistance to B.cinerea.Furthermore,ERF1 A is identified to be a substrate of MPK3 and MPK6,which phosphoactivate ERF1 A to enhance its functions in suppressing ethylene biosynthesis and inducing defensin gene expression.Taken together,our data reveal that ERF1 A and its phosphorylation by MPK3/MPK6 not only mediate the negativefeedback regulation of the B.cinerea-induced ethylene biosynthesis,but also upregulate defensin gene expression to increase Arabidopsis resistance to B.cinerea.