Regulation of systemic acquired resistance by NPR1 and its partners

Abstract

The NPR1 protein of Arabidopsis thaliana has been shown to be an important regulatory component of systemic acquired resistance (SAR). Mutations in the NPR1 gene block the induction of SAR by the signal molecule salicylic acid (SA). NPR1 contains an ankyrin repeats and a BTB domain which are involved in interaction with other protein(s). To further study the function of NPR1 and the regulatory mechanism of SAR, we used both molecular and genetic approaches to identify additional SAR regulatory components. Through a yeast two-hybrid screen we found that NPR1 interacts specifically with bZIP transcription factors. The involvement of bZIP transcription factors in controlling the SA-induced genes had been suggested by a number of promoter studies performed on these genes. It was found that as1 element, which is a binding site for bZIP transcription factors, is essential for SA-induced gene expression. In a genetic screen for suppressors of npr1, we found a mutant, sni1, that restored the responsiveness to SAR induction in npr1. The genetic characteristics of the sni1 mutant and the sequence of SNI1 suggest that the wild-type SNI1 protein is a negative regulator of SAR. We believe that SAR is controlled by both positive regulators and negative regulators.