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.