Premium
Capsicum annuum WRKY protein CaWRKY1 is a negative regulator of pathogen defense
Author(s) -
Oh SangKeun,
Baek KwangHyun,
Park Jeong Mee,
Yi So Young,
Yu Seung Hun,
Kamoun Sophien,
Choi Doil
Publication year - 2008
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2007.02310.x
Subject(s) - wrky protein domain , biology , hypersensitive response , pathogen , systemic acquired resistance , plant defense against herbivory , gene silencing , pepper , transgene , gene , microbiology and biotechnology , genetically modified crops , npr1 , plant disease resistance , genetics , gene expression , arabidopsis , horticulture , transcriptome , mutant , medicine , heart failure , natriuretic peptide
Summary• 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.