The pepper receptor-like cytoplasmic protein kinase CaPIK1 is involved in plant signaling of defense and cell-death responses

被引:48
作者
Kim, Dae Sung [1 ]
Hwang, Byung Kook [1 ]
机构
[1] Korea Univ, Sch Life Sci & Biotechnol, Lab Mol Plant Pathol, Seoul 136713, South Korea
关键词
pepper; Xanthomonas campestris pv; vesicatoria; RLCK; ROS burst; cell death; plant defense; DISEASE RESISTANCE; INNATE IMMUNITY; NITRIC-OXIDE; GENE FAMILY; ARABIDOPSIS; PERCEPTION; ACTIVATION; RECOGNITION; GENERATION; ELICITOR;
D O I
10.1111/j.1365-313X.2011.04525.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
P>Certain protein kinases have been shown to be crucial for plant cell signaling pathways associated with plant immune responses. Here we identified a pepper (Capsicum annuum) receptor-like cytoplasmic protein kinase (RLCK) gene (CaPIK1) that is transcriptionally activated by infection with Xanthomonas campestris pv. vesicatoria (Xcv). Silencing of CaPIK1 in pepper plants confers enhanced susceptibility to Xcv infection. Salicylic acid-dependent defense responses are attenuated in the CaPIK1-silenced plants, including expression of salicylic acid-dependent genes, but not of a jasmonic acid-regulated gene. Induction of salicylic acid accumulation by Xcv infection is compromised in CaPIK1-silenced plants. The functional CaPIK1 protein not only autophosphorylates, but also phosphorylates myelin basic protein. CaPIK1 exists in the cytoplasm and also localizes to the plasma membrane of plant cells via its N-terminus. Transient expression of CaPIK1 in pepper leaves leads to generation of reactive oxygen species (ROS), ultimately leading to hypersensitive cell death. Over-expression (OX) of CaPIK1 in Arabidopsis enhances the basal resistance to infection with Pseudomonas syringae pv. tomato and Hyaloperonospora arabidopsidis, associated with elevated ROS bursts. Salicylic acid levels in CaPIK1-OX plants are higher than those in wild-type plants. Together, these results suggest that CaPIK1 modulates the signaling required for the salicylic acid-dependent defense response to pathogen infection.
引用
收藏
页码:642 / 655
页数:14
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