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Published on April 3, 2003; 10.1104/pp.102.018887

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Received December 9, 2002
Returned for revision January 20, 2003
Accepted February 19, 2003

Ethylene Insensitivity Modulates Ozone-Induced Cell Death in Birch

Jorma Vahala , Raili Ruonala , Markku Keinänen , Hannele Tuominen , and Jaakko Kangasjärvi *

Institute of Biotechnology and Department of Biosciences, University of Helsinki, POB 56 (Viikinkaari 9), FIN-00014 Helsinki, Finland (J.V., R.R., M.K., H.T., J.K.); Department of Applied Biology, University of Helsinki, POB 27 (Latokartanonkaari 5-7), FIN-00014 Helsinki, Finland (J.V.); and Laboratory of Plant Physiology and Molecular Biology, Department of Biology, University of Turku, FIN-20014 Turku, Finland (J.K.)

* Corresponding author; email: jaakko.kangasjarvi{at}helsinki.fi.

We have used genotypic variation in birch (Betula pendula Roth) to investigate the roles of ozone (O3)-induced ethylene (ET), jasmonic acid, and salicylic acid in the regulation of tissue tolerance to O3. Of these hormones, ET evolution correlated best with O3-induced cell death. Disruption of ET perception by transformation of birch with the dominant negative mutant allele etr1-1 of the Arabidopsis ET receptor gene ETR1 or blocking of ET perception with 1-methylcyclopropene reduced but did not completely prevent the O3-induced cell death, when inhibition of ET biosynthesis with aminooxyacetic acid completely abolished O3 lesion formation. This suggests the presence of an ET-signaling-independent but ET biosynthesis-dependent component in the ET-mediated stimulation of cell death in O3-exposed birch. Functional ET signaling was required for the O3 induction of the gene encoding {beta}-cyanoalanine synthase, which catalyzes detoxification of the cyanide formed during ET biosynthesis. The results suggest that functional ET signaling is required to protect birch from the O3-induced cell death and that a decrease in ET sensitivity together with a simultaneous, high ET biosynthesis can potentially cause cell death through a deficient detoxification of cyanide.




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