Disease resistance gene-induced growth inhibition is enhanced by rcd1 independent of defense activation in Arabidopsis.

Activation of plant immune responses is often associated with an inhibition of plant growth. The molecular mechanisms underlying this fitness cost are unknown. Here, we utilize the autoimmune response mutant suppressor of npr1, constitutive1 (snc1) resulting from an activated form of the Disease Resistance (R) gene to dissect the genetic component mediating growth inhibition in Arabidopsis (Arabidopsis thaliana). The radical-induced cell death1 (rcd1) mutant defective in responses to reactive oxygen species (ROS) was isolated as an enhancer of the snc1 mutant in growth inhibition but not in defense response activation. Similarly, the vitamin C2 (vtc2) and vtc3 mutants defective in ROS detoxification enhanced the growth defects of snc1. Thus, perturbation of ROS status by R gene activation is responsible for the growth inhibition, and this effect is independent of defense response activation. This was further supported by the partial rescue of growth defects of rcd1 snc1 by the respiratory burst oxidase homolog D (rbohD) and rbohF mutations compromising the generation of ROS burst. Collectively, these findings indicate that perturbation of ROS homeostasis contributes to the fitness cost independent of defense activation.