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STRESS INDUCED FACTOR 2 Regulates Arabidopsis Stomatal Immunity through Phosphorylation of the Anion Channel SLAC1

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SIF2 is critical for Arabidopsis (Arabidopsis thaliana) resistance to bacteria by regulating stomatal immunity, belongs to the FLS2/BAK1 immunity receptor complex, and phosphorylates the anion channel SLAC1. Upon recognition of… Click to show full abstract

SIF2 is critical for Arabidopsis (Arabidopsis thaliana) resistance to bacteria by regulating stomatal immunity, belongs to the FLS2/BAK1 immunity receptor complex, and phosphorylates the anion channel SLAC1. Upon recognition of microbes, pattern recognition receptors (PRRs) activate pattern-triggered immunity. FLAGELLIN SENSING2 (FLS2) and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1) form a typical PRR complex that senses bacteria. Here, we report that the kinase activity of the malectin-like receptor-like kinase STRESS INDUCED FACTOR 2 (SIF2) is critical for Arabidopsis (Arabidopsis thaliana) resistance to bacteria by regulating stomatal immunity. SIF2 physically associates with the FLS2-BAK1 PRR complex and interacts with and phosphorylates the guard cell SLOW ANION CHANNEL1 (SLAC1), which is necessary for abscisic acid (ABA)-mediated stomatal closure. SIF2 is also required for the activation of ABA-induced S-type anion currents in Arabidopsis protoplasts, and SIF2 is sufficient to activate SLAC1 anion channels in Xenopus oocytes. SIF2-mediated activation of SLAC1 depends on specific phosphorylation of Ser 65. This work reveals that SIF2 functions between the FLS2-BAK1 initial immunity receptor complex and the final actuator SLAC1 in stomatal immunity.

Keywords: immunity; anion channel; slac1; stomatal immunity; arabidopsis

Journal Title: Plant Cell
Year Published: 2020

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