Lee Dong Sook, Kim Young Cheon, Kwon Sun Jae, Ryu Choong-Min, Park Ohkmae K
Department of Life Sciences, Korea University, Seoul, South Korea.
Molecular Phytobacteriology Laboratory, KRIBB, Daejeon, South Korea.
Front Plant Sci. 2017 Oct 27;8:1856. doi: 10.3389/fpls.2017.01856. eCollection 2017.
Receptor-like kinases are important signaling components that regulate a variety of cellular processes. In this study, an Arabidopsis cDNA microarray analysis led to the identification of the cysteine-rich receptor-like kinase CRK36 responsive to the necrotrophic fungal pathogen, . To determine the function of in plant immunity, T-DNA-insertion knockdown () and overexpressing () plants were prepared. plants exhibited increased hypersensitive cell death and ROS burst in response to avirulent pathogens. Treatment with a typical pathogen-associated molecular pattern, flg22, markedly induced pattern-triggered immune responses, notably stomatal defense, in plants. The immune responses were weakened in plants. Protein-protein interaction assays revealed the association of CRK36, FLS2, and BIK1. CRK36 enhanced flg22-triggered BIK1 phosphorylation, which showed defects with Cys mutations in the DUF26 motifs of CRK36. Disruption of and genes further impaired CRK36-mediated stomatal defense. We propose that CRK36, together with BIK1 and NADPH oxidases, may form a positive activation loop that enhances ROS burst and leads to the promotion of stomatal immunity.
类受体激酶是调节多种细胞过程的重要信号组分。在本研究中,通过拟南芥cDNA微阵列分析鉴定出一种对坏死营养型真菌病原体有响应的富含半胱氨酸的类受体激酶CRK36。为了确定其在植物免疫中的功能,制备了T-DNA插入敲除()和过表达()植株。植株对无毒病原体表现出超敏细胞死亡增加和活性氧爆发。用典型的病原体相关分子模式flg22处理,能显著诱导植株的模式触发免疫反应,尤其是气孔防御。植株的免疫反应减弱。蛋白质-蛋白质相互作用分析揭示了CRK36、FLS2和BIK1之间的关联。CRK36增强了flg22触发的BIK1磷酸化,而CRK36的DUF26基序中的半胱氨酸突变则显示出缺陷。和基因的破坏进一步损害了CRK36介导的气孔防御。我们提出,CRK36与BIK1和NADPH氧化酶一起,可能形成一个正激活环,增强活性氧爆发并促进气孔免疫。