Capsicum annuum WRKY protein CaWRKY1 is a negative regulator of pathogen defense

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Title
Capsicum annuum WRKY protein CaWRKY1 is a negative regulator of pathogen defense
Author(s)
Sang-Keun Oh; K H Baek; Jeong Mee Park; S Y Yi; S H Yu; S Kamoun; Doil Choi
Bibliographic Citation
New Phytologist, vol. 177, no. 4, pp. 977-989
Publication Year
2008
Abstract
Plants respond to pathogens by regulating a network of signaling pathways that fine-tune transcriptional activation of defense-related genes. ? The aim of this study was to determine the role of Capsicum annuum WRKY zinc finger-domain transcription factor 1 (CaWRKY1) in defense. In previous studies, CaWRKY1 was found to be rapidly induced in C. annuum (chili pepper) leaves by incompatible and compatible pathogen inoculations, but the complexity of the network of the WRKY family prevented the function of CaWRKY1 in defense from being elucidated. ? Virus-induced gene silencing of CaWRKY1 in chili pepper leaves resulted in decreased growth of Xanthomonas axonopodis pv. vesicatoria race 1. CaWRKY1-overexpressing transgenic plants showed accelerated hypersensitive cell death in response to infection with tobacco mosaic virus and Pseudomonas syringe pv. tabaci. Lower levels of pathogenesis-related gene induction were observed in CaWRKY1-overexpressing transgenic plants following salicylic acid (SA) treatments. ? This work suggests that the newly characterized CaWRKY1, which is strongly induced by pathogen infections and the signal molecule SA, acts as a regulator to turn off systemic acquired resistance once the pathogen challenge has diminished and to prevent spurious activation of defense responses at suboptimal concentrations of SA.
Keyword
Chili pepper (Capsicum annuum)Disease resistanceHypersensitive responsePlant defenseSystemic acquired resistanceWRKY transcription factor
ISSN
0028-646X
Publisher
Wiley
DOI
http://dx.doi.org/10.1111/j.1469-8137.2007.02310.x
Type
Article
Appears in Collections:
Division of Research on National Challenges > Plant Systems Engineering Research > 1. Journal Articles
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