The Sainsbury Laboratory, Norwich Research Park, NR4 7UH Norwich, UK.
Department of Plant Biochemistry, Dahlem Centre of Plant Sciences, Freie Universität Berlin, 14195 Berlin, Germany.
Cell Host Microbe. 2014 Nov 12;16(5):605-15. doi: 10.1016/j.chom.2014.10.007.
Plant perception of pathogen-associated molecular patterns (PAMPs) triggers a phosphorylation relay leading to PAMP-triggered immunity (PTI). Despite increasing knowledge of PTI signaling, how immune homeostasis is maintained remains largely unknown. Here we describe a forward-genetic screen to identify loci involved in PTI and characterize the Arabidopsis calcium-dependent protein kinase CPK28 as a negative regulator of immune signaling. Genetic analyses demonstrate that CPK28 attenuates PAMP-triggered immune responses and antibacterial immunity. CPK28 interacts with and phosphorylates the plasma-membrane-associated cytoplasmic kinase BIK1, an important convergent substrate of multiple pattern recognition receptor (PRR) complexes. We find that BIK1 is rate limiting in PTI signaling and that it is continuously turned over to maintain cellular homeostasis. We further show that CPK28 contributes to BIK1 turnover. Our results suggest a negative regulatory mechanism that continually buffers immune signaling by controlling the turnover of this key signaling kinase.
植物对病原体相关分子模式（PAMPs）的感知触发了一个磷酸化传递，导致病原体触发的免疫（PTI）。尽管对 PTI 信号的了解越来越多，但免疫稳态是如何维持的仍然知之甚少。在这里，我们描述了一个正向遗传筛选，以鉴定参与 PTI 的基因座，并将拟南芥钙依赖性蛋白激酶 CPK28 鉴定为免疫信号的负调节剂。遗传分析表明，CPK28 减弱了 PAMP 触发的免疫反应和抗菌免疫。CPK28 与质膜相关的细胞质激酶 BIK1 相互作用并磷酸化 BIK1，BIK1 是多种模式识别受体（PRR）复合物的一个重要汇聚底物。我们发现 BIK1 在 PTI 信号转导中是限速的，它不断被降解以维持细胞内稳态。我们进一步表明 CPK28 有助于 BIK1 的降解。我们的结果表明，通过控制这种关键信号激酶的周转，CPK28 提供了一种负调控机制，持续缓冲免疫信号。
