Involvement of ethylene in lesion development and systemic acquired resistance in tobacco during the hypersensitive reaction to tobacco mosaic virus

Different approaches were taken to investigate the significance of ethylene in lesion development and systemic acquired resistance (SAR) in tobacco (Nicotiana tabacum) reacting hypersensitively to tobacco mosaic virus (TMV). Gaseous ethylene, the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) and the ethylene releasing compound ethephon all reduced primary lesion size when applied before or shortly after virus inoculation. Inhibiting TMV-induced ethylene production in primary infected leaves by the inhibitor of ACC-synthase 1-aminoethoxyvinylglycine, the inhibitor of ACC-oxidase cobalt chloric, or the inhibitors of ethylene action silver nitrate and 2,5-norbornadiene (N-BD) also reduced lesion expansion, The results support Previous findings that exposure of leaves to ethylene or ethylene-releasing compounds prior to inoculation causes an early cessation of lesion growth, whereas ethylene synthesized during lesion development contributes to continued lesion expansion. Local treatment,vith ethtephon-induced systemic resistance, whereas treatment with NBD of a primary TMV-inoculated leaf tended to reduce the, extent of SAR attained in both upper and lower leaves. Transgenic plants, with modulated ethylene levels obtained through expression of sense or antisense ACC-synthase RNA did not show alterations in Primary T-MV lesion size or SAR, apparently because ethylene production was not altered sufficiently to affect lesion development. In contrast, the use of ethylene insensitive (Tetr) plants, transformed with a mutant etrl-1 gene from Arabidopsis, confirmed that virus-induced ethylene promotes lesion expansion and demonstrated that the hormone contributes to the level of SAR attained. In the Ten, plants the SAR response was substantially reduced. The results indicate that in tobacco ethylene perception is involved in lesion expansion, as well as in the generation and/or release of the mobile signal that induces SAR in non-infected plant parts. (C) 2001 Academic Press.