Ethylene Insensitivity Modulates Ozone-Induced Cell Death in Birch1

AUTOR(ES)

Vahala, Jorma

FONTE

American Society of Plant Biologists

RESUMO

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 β-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.

Documentos Relacionados

• Jasmonic Acid Signaling Modulates Ozone-Induced Hypersensitive Cell Death
• Ozone-Induced Programmed Cell Death in the Arabidopsis radical-induced cell death1 Mutant1
• Ozone-Induced Cell Death in Tobacco Cultivar Bel W3 Plants. The Role of Programmed Cell Death in Lesion Formation
• Senescence-Associated Gene Expression during Ozone-Induced Leaf Senescence in Arabidopsis1
• Hydrogen Peroxide Activates Cell Death and Defense Gene Expression in Birch1