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Plant Cell, Vol. 12, 1849-1862, October 2000, Copyright © 2000, American Society of Plant Physiologists
Ozone-Sensitive Arabidopsis rcd1 Mutant Reveals Opposite Roles for Ethylene and Jasmonate Signaling Pathways in Regulating Superoxide-Dependent Cell Death
Kirk Overmyera,
Hannele Tuominena,
Reetta Kettunena,
Christian Betzb,
Christian Langebartelsb,
Heinrich Sandermann, Jr.b, and
Jaakko Kangasjärvia
a Institute of Biotechnology and Department of Biosciences, University of Helsinki, POB 56 (Viikinkaari 5 D), FIN-00014 Helsinki, Finland
b Institute of Biochemical Plant Pathology, GSF Research Center for Environment and Health, D-85764 Oberschleissheim, Germany
Correspondence to:
Jaakko Kangasjärvi, jaakko.kangasjarvi{at}helsinki.fi (E-mail), 358-9-191-59-079 (fax)
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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