FIG. 7.

Proposed model for the role of HRL1 in defense signaling. (A) In wild-type plants, HRL1 is involved in Coenzyme Q₁₀ (CoQ) biosynthesis. CoQ acts in the mitochondrial electron transport chain (ETC) as an electron carrier by getting cyclically reduced (ubiquinol) and oxidized (ubiquinone). This electron carrier function ensures loss of minimal electrons during the oxidation/reduction process that contributes toward generation of ROS. The physiological ROS pool creates a threshold ROS level that enables effective oxidative bursts during defense against pathogens. (B) In hrl1 mutants, reduced levels of CoQ compromise effective quenching of free electrons, thereby increasing electrons available for ROS production. These enhanced ROS levels contribute to activation of constitutive defense against pathogens along with a free radical-induced lesion phenotype, both of which are hallmarks of hrl1 mutant plants. (C) In HRL1 overexpression plants, increased levels of CoQ effectively quench free electrons, thereby reducing electrons available for ROS production. These reduced ROS levels lead to sub-optimal oxidative bursts required for effective defense against pathogens and thus the enhanced susceptibility against pathogens in these HRL1 overexpressing plants. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars