Ozone-Sensitive Arabidopsis rcd1 Mutant Reveals Opposite Roles for Ethylene and Jasmonate Signaling Pathways in Regulating Superoxide-Dependent Cell Death

Abstract

We have isolated a codominant Arabidopsis mutant, radical-induced cell death1 (rcd1), in which ozone (O3) and extracellular superoxide (O2 •–), but not hydrogen peroxide, induce cellular O2 •– accumulation and transient spreading lesions. The cellular O2 •– accumulation is ethylene dependent, occurs ahead of the expanding lesions before visible symptoms appear, and is required for lesion propagation. Exogenous ethylene increased O2 •–-dependent cell death, whereas impairment of ethylene perception by norbornadiene in rcd1 or ethylene insensitivity in the ethylene-insensitive mutant ein2 and in the rcd1 ein2 double mutant blocked O2 •– accumulation and lesion propagation. Exogenous methyl jasmonate inhibited propagation of cell death in rcd1. Accordingly, the O3-exposed jasmonate-insensitive mutant jar1 displayed spreading cell death and a prolonged O2 •– accumulation pattern. These results suggest that ethylene acts as a promoting factor during the propagation phase of developing oxyradical-dependent lesions, whereas jasmonates have a role in lesion containment. Interaction and balance between these pathways may serve to fine-tune propagation and containment processes, resulting in alternate lesion size and formation kinetics.