CRY1 couples blue light dependent systemic acquired defense through NPR1 interaction and SnRK3.6-mediated translocation

Abstract Systemic acquired resistance (SAR) is a whole-plant immune response triggered by localized infection. Cryptochromes (CRY) that are blue light receptors, work together with phytochromes (PHY) to regulate light dependent responses in Arabidopsis. Although the effect of light on plant immunity is fairly well studied, the molecular mechanisms remain unclear. In this study, we show that CRY1 is essential for optimal SAR induction under blue light conditions in Arabidopsis thaliana . The cry1 mutants fail to activate SAR under blue light, as evidenced by reduced expression of defense genes, increased susceptibility to Pseudomonas syringae ( Pst DC3000), and impaired stomatal defense. While SAR is intact in both wild type and cry1 under white light, blue light selectively reveals critical role of CRY1 in SAR. Interestingly, npr1 mutants activate SAR under blue light, supporting the fact that blue light can trigger SAR through NPR1 independent pathways. Using biochemical and cell-based assays, we show that CRY1 directly interacts with NPR1 in nucleus in a blue-light–enhanced manner. Overexpression of CRY1 induces NPR1 levels and enhances SAR. Expression of each of them individually partly rescued SAR, but their co-expression fully reinstated it, implying that SAR relies on interaction between NPR1 and CRY1. Stomatal movement measurements further show that CRY1 and NPR1 act synergistically to promote stomatal closure to limit pathogen entry. We also identify SnRK3.6, a blue-light-inducible kinase, as a novel regulator of CRY1. SnRK3.6 physically interacts with and phosphorylates CRY1, facilitating its nuclear translocation. Our results revealed a novel role of CRY1-NPR1 complex formation and regulation of CRY1 by SnRK3.6 in inducing SAR.