A NAC transcription factor and SNI1 cooperatively suppress basal pathogen resistance in Arabidopsis thaliana

Cited 45 time in scopus
Metadata Downloads
Title
A NAC transcription factor and SNI1 cooperatively suppress basal pathogen resistance in Arabidopsis thaliana
Author(s)
Ho Soo Kim; H C Park; K E Kim; M S Jung; H J Han; S H Kim; Y S Kwon; S Bahk; J An; D W Bae; D J Yun; Sang Soo Kwak; W S Chung
Bibliographic Citation
Nucleic Acids Research, vol. 40, no. 18, pp. 9182-9192
Publication Year
2012
Abstract
Transcriptional repression of pathogen defense-related genes is essential for plant growth and development. Several proteins are known to be involved in the transcriptional regulation of plant defense responses. However, mechanisms by which expression of defense-related genes are regulated by repressor proteins are poorly characterized. Here, we describe the in planta function of CBNAC, a calmodulin-regulated NAC transcriptional repressor in Arabidopsis. A T-DNA insertional mutant (cbnac1) displayed enhanced resistance to a virulent strain of the bacterial pathogen Pseudomonas syringae DC3000 (PstDC3000), whereas resistance was reduced in transgenic CBNAC overexpression lines. The observed changes in disease resistance were correlated with alterations in pathogenesis-related protein 1 (PR1) gene expression. CBNAC bound directly to the PR1 promoter. SNI1 (suppressor of nonexpressor of PR genes1, inducible 1) was identified as a CBNAC-binding protein. Basal resistance to PstDC3000 and derepression of PR1 expression was greater in the cbnac1 sni1 double mutant than in either cbnac1 or sni1 mutants. SNI1 enhanced binding of CBNAC to its cognate PR1 promoter element. CBNAC and SNI1 are hypothesized to work as repressor proteins in the cooperative suppression of plant basal defense.
ISSN
0305-1048
Publisher
Oxford Univ Press
DOI
http://dx.doi.org/10.1093/nar/gks683
Type
Article
Appears in Collections:
Division of Research on National Challenges > Plant Systems Engineering Research > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.