9182–9192 Nucleic Acids Research, 2012, Vol. 40, No. 18 doi:10.1093/nar/gks683 Published online 22 July 2012 A NAC transcription factor and SNI1 cooperatively suppress basal pathogen resistance in Arabidopsis thaliana Ho Soo Kim1,2, Hyeong Cheol Park3, Kyung Eun Kim1,3, Mi Soon Jung 3 , Hay Ju Han 1 , Sun Ho Kim3, Young Sang Kwon 1 , Sunghwa Bahk 1 , Jonguk An 1 , Dong Won Bae 4 , Dae-Jin Yun1,3, Sang-Soo Kwak2 and Woo Sik Chung1,3,* 1Division of Applied Life Science (BK21 Program), Gyeongsang National University, Jinju 660-701, 2Environmental Biotechnology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yusong-gu, Daejeon 305-806, 3Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 660-701 and 4Central Instrument Facility, Gyeongsang National University, Jinju 660-701, Korea Received April 13, 2012; Revised and Accepted June 20, 2012 ABSTRACT Transcriptional repression of pathogen defense- related genes is essential for plant growth and de- velopment. 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 chara- cterized. Here, we describe the in planta function of CBNAC, a calmodulin-regulated NAC transcrip- tional 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. INTRODUCTION Plants, unlike animals, do not possess specialized cells for protection against invading pathogens. When a pathogen challenge is detected, plant defense responses occur through the activation of cellular signal transduction pathways leading to global transcriptional repro- gramming. These changes favor immune responses over normal cellular functions (1,2). Equally important is the suppression of immune responses in the absence of a pathogen threat that is necessary for proper plant growth and development. Thus, the induction of defense response to a speciﬁc pathogen occurs by a complex sig- naling network interconnected by crosstalk with networks that regulate response to other stressors, growth and de- velopment (3). Research on Arabidopsis thaliana has demonstrated that local and systemic resistance responses to biotrophic pathogens such as Pseudomonas syringae are mediated by the plant hormone salicylic acid (SA). Accumulation of SA leads to reduction of the oligomeric cytoplasmic form of the transcriptional co-activator NPR1/NIM1 (nonexpressor of PR genes1) to a monomeric form that translocates to the nucleus (4–8). Once there, NPR1 interacts with three redundant transcription factors, TGA2, TGA5 and TGA6 to activate expression of defense genes such as pathogenesis-related protein 1 (PR1) (9–13). Constitutive activation of defense is detrimental to the normal growth of plants (14–17). Therefore, negative regulation of defense responses is very important. Negative regulators of the PR1 expression and resistance to P. syringae include SNI1 (suppressor of npr1-1, inducible1), NIM1-interacting1 and several WRKY *To whom correspondence should be addressed. Tel: +82 55 772 1363; Fax: +82 55 759 9363; Email: chungws@gnu.ac.kr The authors wish it to be known that, in their opinion, the ﬁrst three authors should be regarded as joint First Authors. The Author(s) 2012. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/ by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.