Department of Plant, Soil and Microbial Sciences, Michigan State University, East Lansing, MI, 48824, USA.
Department of Plant Biology, Michigan State University, East Lansing, MI, 48824, USA.
Nat Commun. 2020 Dec 4;11(1):6234. doi: 10.1038/s41467-020-20007-4.
Pattern-triggered immunity and effector-triggered immunity are two primary forms of innate immunity in land plants. The molecular components and connecting nodes of pattern-triggered immunity and effector-triggered immunity are not fully understood. Here, we report that the Arabidopsis calcium-dependent protein kinase CPK3 is a key regulator of both pattern-triggered immunity and effector-triggered immunity. In vitro and in vivo phosphorylation assays, coupled with genetic and cell biology-based analyses, show that actin-depolymerization factor 4 (ADF4) is a physiological substrate of CPK3, and that phosphorylation of ADF4 by CPK3 governs actin cytoskeletal organization associated with pattern-triggered immunity. CPK3 regulates stomatal closure induced by flg22 and is required for resistance to Pst DC3000. Our data further demonstrates that CPK3 is required for resistance to Pst DC3000 carrying the effector AvrPphB. These results suggest that CPK3 is a missing link between cytoskeleton organization, pattern-triggered immunity and effector-triggered immunity.
模式触发免疫和效应器触发免疫是陆地植物先天免疫的两种主要形式。模式触发免疫和效应器触发免疫的分子组成和连接节点尚未完全了解。在这里，我们报告拟南芥钙依赖蛋白激酶 CPK3 是模式触发免疫和效应器触发免疫的关键调节剂。体外和体内磷酸化测定，以及基于遗传和细胞生物学的分析表明，肌动蛋白解聚因子 4 (ADF4) 是 CPK3 的生理底物，CPK3 对 ADF4 的磷酸化控制与模式触发免疫相关的肌动蛋白细胞骨架组织。CPK3 调节 flg22 诱导的气孔关闭，并需要抵抗 Pst DC3000。我们的数据进一步表明，CPK3 是抵抗携带效应物 AvrPphB 的 Pst DC3000 所必需的。这些结果表明，CPK3 是细胞骨架组织、模式触发免疫和效应器触发免疫之间缺失的联系。
