Abstract
The Arabidopsis nsl2 (necrotic spotted lesion 2) mutant, which has been originally reported as the cad1 (constitutively activated cell death 1), shows a phenotype that mimics a hypersensitive response (HR)-like cell death. The NSL2 protein is suggested to negatively control the salicylic acid (SA)-mediated pathway of HR-like cell death in plant immunity. The induction of systemic acquired resistance (SAR) results in the induction of pathogenesis-related (PR) genes in systemic organs triggered by the local HR. In this report, we establish a NSL2 knockdown system in transgenic Arabidopsis based on constitutive or dexamethasone (DEX)-induced RNAi. The former showed a nsl2-like phenotype. In DEX-induced RNAi, localized knockdown resulted in the induction of PR1 gene expression and the restriction of bacterial growth in both DEX-treated and systemic leaves. These results indicate that NSL2 negatively controls SAR via HR.
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