Abstract
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.
Highlights
Plants are exposed to a constant and diverse array of potential microbial pathogens and have developed the ability to protect themselves from pathogen attack by the early detection of disease-causing agents (Kenrick and Crane, 1997; Jones and Dangl, 2006)
The results suggest that CaChitIV positively regulates CaPIK1-triggered cell death and defence responses through its interaction with CaPIK1
The results suggest that CaChitIV positively regulates reactive oxygen species (ROS) and nitric oxide (NO) burst, leading to plant cell death and defence responses through its interaction with CaPIK1
Summary
Plants are exposed to a constant and diverse array of potential microbial pathogens and have developed the ability to protect themselves from pathogen attack by the early detection of disease-causing agents (Kenrick and Crane, 1997; Jones and Dangl, 2006). In a previous study (Kim and Hwang, 2011), the pepper receptor-like cytoplasmic protein kinase, CaPIK1, which mediates signalling of cell death and defence responses to microbial pathogens was identified. It is known that plant chitinases play important roles in defence against pathogenic attacks (Gomez et al, 2002; Hong and Hwang, 2002; Hietala et al, 2004) and stress response (Hong and Hwang, 2006; Takenaka et al, 2009), and in growth and development (Wiweger et al, 2003). The pathogen-induced CaPIK1 (pepper receptor-like cytoplasmic protein kinase) was identified as a positive regulator of plant cell death and defence responses (Kim and Hwang, 2011). The results suggest that CaChitIV positively regulates ROS and NO burst, leading to plant cell death and defence responses through its interaction with CaPIK1
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