The Capsicum annuum class IV chitinase ChitIV interacts with receptor-like cytoplasmic protein kinase PIK1 to accelerate PIK1-triggered cell death and defence responses.
The Capsicum annuum class IV chitinase ChitIV interacts with receptor-like cytoplasmic protein kinase PIK1 to accelerate PIK1-triggered cell death and defence responses.
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DOI：
10.1093/jxb/erv001
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发表时间：
2015-04
影响因子：
6.9
通讯作者：
Hwang BK
中科院分区：
文献类型：
--
作者：
Kim DS;Kim NH;Hwang BK
辣椒IV类几丁质酶CaChitIV与辣椒受体样细胞质蛋白激酶CaPIK 1相互作用，促进CaPIK 1触发的细胞死亡和防御反应。CaChitIV定位于内质网。辣椒受体样细胞质蛋白激酶，CaPIK 1，介导的植物细胞死亡和防御反应的信号转导先前被确定。在这里，鉴定的IV类几丁质酶，CaChitIV，从辣椒植物（辣椒），它与CaPIK 1相互作用，促进CaPIK 1触发的细胞死亡和防御反应，报告。CaChitIV含有信号肽、几丁质结合结构域和乙二醇水解酶结构域。CaChitIV的表达被野油菜黄单胞菌致病变种上调。水疱病（Xcv）感染。值得注意的是，无毒Xcv感染迅速诱导辣椒叶片中CaChitIV的表达。双分子荧光互补和免疫共沉淀显示，CaPIK 1与CaChitIV在植物中相互作用，并且CaPIK 1-CaChitIV复合物主要定位于细胞质和质膜。CaChitIV也定位于内质网中。CaChitIV与CaPIK 1的瞬时共表达增强了CaPIK 1触发的细胞死亡反应以及活性氧（ROS）和一氧化氮（NO）爆发。辣椒植物中CaChitIV和CaPIK 1的共沉默赋予了对Xcv感染的增强的易感性，这伴随着细胞死亡反应、ROS和NO爆发以及防御反应基因的诱导减少。CaPIK 1在拟南芥中的异位表达增强了拟南芥对透明霜霉感染的基础抗性。总之，结果表明，CaChitIV通过与CaPIK 1的相互作用积极调节CaPIK 1触发的细胞死亡和防御反应。
The pepper class IV chitinase CaChitIV interacts with the pepper receptor-like cytoplasmic protein kinase CaPIK1 and promotes CaPIK1-triggered cell death and defence responses. CaChitIV is localized to the endoplasmic reticulum. The pepper receptor-like cytoplasmic protein kinase, CaPIK1, which mediates signalling of plant cell death and defence responses was previously identified. Here, the identification of a class IV chitinase, CaChitIV, from pepper plants (Capsicum annuum), which interacts with CaPIK1 and promotes CaPIK1-triggered cell death and defence responses, is reported. CaChitIV contains a signal peptide, chitin-binding domain, and glycol hydrolase domain. CaChitIV expression was up-regulated by Xanthomonas campestris pv. vesicatoria (Xcv) infection. Notably, avirulent Xcv infection rapidly induced CaChitIV expression in pepper leaves. Bimolecular fluorescence complementation and co-immunoprecipitation revealed that CaPIK1 interacts with CaChitIV in planta, and that the CaPIK1–CaChitIV complex is localized mainly in the cytoplasm and plasma membrane. CaChitIV is also localized in the endoplasmic reticulum. Transient co-expression of CaChitIV with CaPIK1 enhanced CaPIK1-triggered cell death response and reactive oxygen species (ROS) and nitric oxide (NO) bursts. Co-silencing of both CaChitIV and CaPIK1 in pepper plants conferred enhanced susceptibility to Xcv infection, which was accompanied by a reduced induction of cell death response, ROS and NO bursts, and defence response genes. Ectopic expression of CaPIK1 in Arabidopsis enhanced basal resistance to Hyaloperonospora arabidopsidis infection. Together, the results suggest that CaChitIV positively regulates CaPIK1-triggered cell death and defence responses through its interaction with CaPIK1.
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