Ozone-sensitive Arabidopsis rcd1 mutant reveals opposite roles for ethylene and jasmonate signaling pathways in regulating superoxide-dependent cell death

We have isolated a codominant Arabidopsis mutant, radical-induced cell death1 (rcd1), in which ozone (O-3) and extracellular superoxide (O-2(.-)), but not hydrogen peroxide, induce cellular O-2(.-) accumulation and transient spreading lesions. The cellular O-2(.-) accumulation is ethylene dependent, occurs ahead of the expanding lesions before visible symptoms appear, and is required for lesion propagation, Exogenous ethylene increased O-2(.-)-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 O-2(.-) accumulation and lesion propagation, Exogenous methyl jasmonate inhibited propagation of cell death in rcd1. Accordingly, the O-3-exposed jasmonate-insensitive mutant jar1 displayed spreading cell death and a prolonged O-2(.-) 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.