Flg22 induces CERK1 phosphorylation

Plant cells employ cell-surface receptors to detect pathogens and launch immunity.Here we show that flg22 can induce a receptor-like kinase CERK1 phosphorylation at juxtamembrane region (JM). However, Genome-wide transcriptional reprogramming and other flg22 responses implied that CERK1 does not directly mediate flg22 signaling. Surprisingly, CERK1 JM phosphorylation can promote chitin responses and fungal resistance for plants and genome-wide transcriptional reprogramming also suggested no sign of constitutive immunity caused by this. Genome-wide survey of the wild type and cerk1 mutant in response to flg22 or transgenic complementation plants of CERK1 and CERK1 mutations植物细胞借助细胞表面受体识别病原体并启动免疫应答。本研究证实，flg22可诱导类受体激酶CERK1在近膜区（juxtamembrane region, JM）发生磷酸化。然而，全基因组转录重编程及其他flg22响应实验结果表明，CERK1并未直接介导flg22信号通路。令人意外的是，CERK1的JM区域磷酸化可增强植物的几丁质响应与真菌抗性；同时全基因组转录重编程分析显示，该修饰并未引发组成型免疫反应。本研究针对野生型植株、cerk1突变体在flg22诱导下的样本，以及携带CERK1及其突变体的转基因互补植株开展了全基因组水平的分析。