Open AccessThe Pepper Calmodulin Gene CaCaM1 Is Involved in Reactive Oxygen Species and Nitric Oxide Generation Required for Cell Death and the Defense Response
Author(s) -
Hyong Woo Choi,
Dong Hyuk Lee,
Byung Kook Hwang
Publication year - 2009
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi-22-11-1389
Subject(s) - nitric oxide , reactive oxygen species , calmodulin , pepper , programmed cell death , biology , nitric oxide synthase , microbiology and biotechnology , chemistry , botany , biochemistry , apoptosis , endocrinology , enzyme , horticulture
Calcium signaling has emerged as an important signal transduction pathway of higher plants in response to biotic and abiotic stresses. Ca 2+ -bound calmodulin (CaM) plays a critical role in decoding and transducing stress signals by activating specific targets. Here, we isolated and functionally characterized the pathogen-responsive CaM gene, Capsicum annuum calmodulin 1 (CaCaM1), from pepper (C. annuum) plants. The cellular function of CaCaM1 was verified by Agrobacterium spp.-mediated transient expression in pepper and transgenic overexpression in Arabidopsis thaliana. Agrobacterium spp.-mediated transient expression of CaCaM1 activated reactive oxygen species (ROS), nitric oxide (NO) generation, and hypersensitive response (HR)-like cell death in pepper leaves, ultimately leading to local acquired resistance to Xanthomonas campestris pv. vesicatoria. CaCaM1-overexpression (OX) Arabidopsis exhibited enhanced resistance to Pseudomonas syringae and Hyaloperonospora parasitica, which was accompanied by enhanced ROS and NO generation and HR-like cell death. Treatment with the calcium-channel blocker suppressed the oxidative and NO bursts and HR-like cell death that were triggered by CaCaM1 expression in pepper and Arabidopsis, suggesting that calcium influx is required for the activation of CaCaM1-mediated defense responses in plants. Upon treatment with the CaM antagonist, virulent P. syringae pv. tomato-induced NO generation was also compromised in CaCaM1-OX leaves. Together, these results suggest that the CaCaM1 gene functions in ROS and NO generation are essential for cell death and defense responses in plants.