Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induced resistance in Arabidopsis

Disease resistance in Arabidopsis is regulated by multiple signal transduct ion pathways in which salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) function as key signaling molecules. Epistasis analyses were performe d between mutants that disrupt these pathways (npr1, eds5, ein2, and jar1) and mutants that constitutively activate these pathways (cpr1, cpr5, and cp r6), allowing exploration of the relationship between the SA- and JA/ET-med iated resistance responses. Two important findings were made. First, the co nstitutive disease resistance exhibited by cpr1, cpr5, and cpr6 is complete ly suppressed by the SA-deficient eds5 mutant but is only partially affecte d by the SA-insensitive npr1 mutant. Moreover, eds5 suppresses the SA-accum ulating phenotype of the cpr mutants, whereas npr1 enhances it. These data indicate the existence of an SA-mediated, NPR1-independent resistance respo nse. Second, the ET-insensitive mutation ein2 and the JA-insensitive mutati on jar1 suppress the NPR1-independent resistance response exhibited by cpr5 and cpr6. Furthermore, ein2 potentiates SA accumulation in cpr5 and cpr5 n pr1 while dampening SA accumulation in cpr6 and cpr6 npr1. These latter res ults indicate that cpr5 and cpr6 regulate resistance through distinct pathw ays and that SA-mediated, NPR1-independent resistance works in combination with components of the JA/ET-mediated response pathways.