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

Authors
Kim, Dae SungHwang, Byung Kook
Issue Date
May-2011
Publisher
WILEY-BLACKWELL
Keywords
pepper; Xanthomonas campestris pv; vesicatoria; RLCK; ROS burst; cell death; plant defense
Citation
PLANT JOURNAL, v.66, no.4, pp.642 - 655
Indexed
SCIE
SCOPUS
Journal Title
PLANT JOURNAL
Volume
66
Number
4
Start Page
642
End Page
655
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/112501
DOI
10.1111/j.1365-313X.2011.04525.x
ISSN
0960-7412
Abstract
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.
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