A cluster of disease resistance genes in Arabidopsis is coordinately regulated by transcriptional activation and RNA silencing.

The RPP5 (for recognition of Peronospora parasitica 5) locus in the Arabidopsis thaliana Columbia strain contains a cluster of paralogous disease Resistance (R) genes that play important roles in innate immunity. Among the R genes in this locus, RPP4 confers resistance to two races of the fungal pathogen Hyaloperonospora parasitica, while activation of SNC1 (for suppressor of npr1-1, constitutive 1) results in the resistance to another race of H. parasitica and to pathovars of the bacterial pathogen Pseudomonas syringae through the accumulation of salicylic acid (SA). Here, we demonstrate that other Columbia RPP5 locus R genes can be induced by transgenic overexpression of SNC1, which itself is regulated by a positive amplification loop involving SA accumulation. We also show that small RNA species that can target RPP5 locus R genes are produced in wild-type plants and that these R genes can be cosuppressed in transgenic plants overexpressing SNC1. Steady state expression levels of SNC1 increase in some mutants (dcl4-4, ago1-36, and upf1-5) defective in RNA silencing as well as in transgenic plants expressing the P1/Helper Component-Protease viral suppressor of RNA silencing. However, steady state levels of small RNA species do not change in mutants that upregulate SNC1. These data indicate many Columbia RPP5 locus R genes can be coordinately regulated both positively and negatively and suggest that the RPP5 locus is poised to respond to pathogens that disturb RNA silencing.