A novel Arabidopsis CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) mutant with enhanced pathogen-induced cell death and altered receptor processing
A novel Arabidopsis CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) mutant with enhanced pathogen-induced cell death and altered receptor processing
复制标题
DOI：
10.1111/nph.12920
复制
发表时间：
2014-12-01
期刊：
影响因子：
9.4
通讯作者：
Lipka, Volker
中科院分区：
文献类型：
--
作者：
Petutschnig, Elena K.;Stolze, Marnie;Lipka, Volker
植物通过模式识别受体感知微生物相关分子模式 (MAMP) 来检测病原体。模式识别受体复合物在细胞死亡控制中也发挥作用，但其潜在机制尚不清楚。在这里，我们报告了 cerk1-4 的分离，这是拟南芥几丁质受体 CERK1 的一种新型突变等位基因，具有增强的防御反应。我们在大麦白粉病的正向遗传筛选中鉴定了 cerk1-4，并通过病原体测定、突变体杂交和防御途径分析对其进行了表征。对 CERK1 和 CERK1-4 蛋白进行生化分析。 cerk1-4 突变导致 CERK1 胞外域中的氨基酸交换。突变植物保持几丁质信号传导能力，但在病原体攻击时表现出高度诱导的水杨酸浓度和失调的细胞死亡。与几丁质信号传导相反，cerk1-4 表型不需要激酶活性，并且由受体的 N 端部分赋予。 CERK1 经历胞外域脱落，这是动物细胞表面蛋白中众所周知的过程。野生型植物含有全长 CERK1 受体蛋白以及可溶形式的 CERK1 胞外域，而 cerk1-4 植物缺乏 N 末端脱落产物。我们的工作表明，CERK1 在细胞死亡控制中可能具有不依赖于几丁质的作用，并且是植物中胞外域脱落的第一个报道。
Plants detect pathogens by sensing microbe-associated molecular patterns (MAMPs) through pattern recognition receptors. Pattern recognition receptor complexes also have roles in cell death control, but the underlying mechanisms are poorly understood. Here, we report isolation of cerk1-4, a novel mutant allele of the Arabidopsis chitin receptor CERK1 with enhanced defense responses. We identified cerk1-4 in a forward genetic screen with barley powdery mildew and consequently characterized it by pathogen assays, mutant crosses and analysis of defense pathways. CERK1 and CERK1-4 proteins were analyzed biochemically. The cerk1-4 mutation causes an amino acid exchange in the CERK1 ectodomain. Mutant plants maintain chitin signaling capacity but exhibit hyper-inducible salicylic acid concentrations and deregulated cell death upon pathogen challenge. In contrast to chitin signaling, the cerk1-4 phenotype does not require kinase activity and is conferred by the N-terminal part of the receptor. CERK1 undergoes ectodomain shedding, a well-known process in animal cell surface proteins. Wild-type plants contain the full-length CERK1 receptor protein as well as a soluble form of the CERK1 ectodomain, whereas cerk1-4 plants lack the N-terminal shedding product. Our work suggests that CERK1 may have a chitin-independent role in cell death control and is the first report of ectodomain shedding in plants.