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

AUTOR(ES)
FONTE

American Society of Plant Physiologists

RESUMO

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.

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