The TIR-NB-LRR gene SNC1 is regulated at the transcript level by multiple factors.

SNC1 (suppressor of NPR1, constitutive 1) is a haplotype-specific Toll and interleukin-1 receptor-like nucleotide-binding site leucine-rich repeat type of resistance (R)-like gene possibly mediating race-specific disease resistance. Inactivation of its negative regulator BON1 (BONZAI1)/CPN1 and BAP1 genes or upregulation of its expression epigenetically lead to constitutive defense responses and dwarf phenotype. Here, we report an autoactivation of SNC1 by introducing it into Arabidopsis as a transgene. The SNC1 genomic fragment confers a dwarf phenotype induced by defense response upregulation associated with a higher SNC1 transcript level. Analysis of the beta-glucuronidase reporter gene under the control of the SNC1 promoter suggests three modes of regulation on the SNC1 transcript level: a repression by the chromosomal structure, a feedback amplification from SNC1 on its promoter sequences, and a repression by BON1. These regulations appear to be independent of each other. The regulation of SNC1 possibly exemplifies a universally complex control of R genes to ensure a repression of R activation under nonstress conditions and a robust activation of defense responses once the R gene is induced.