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

Abstract

Dierent approaches were taken to investigate the signi®cance 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 chloride, or the inhibitors of ethylene action silver nitrate and 2,5-norbornadiene (NBD) also reduced lesion expansion. The results support previous ®ndings 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 with ethephon-induced systemic resistance, whereas treatment with NBD of a primary TMVinoculated 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 TMV lesion size or SAR, apparently because ethylene production was not altered suciently to aect lesion development. In contrast, the use of ethylene insensitive (Tetr) plants, transformed with a mutant etr1-1 gene from Arabidopsis, con®rmed that virus-induced ethylene promotes lesion expansion and demonstrated that the hormone contributes to the level of SAR attained. In the Tetr 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.*

Nitric Oxide Interacts with Salicylate to Regulate Biphasic Ethylene Production during the Hypersensitive Response

“…Different groups have noted normal HR formation in Arabidopsis (Bent et al, 1992) and tomato (Solanum lycopersicum; Hoffman et al, 1999;Ciardi et al, 2000) lines where ethylene signaling was perturbed. However, HR-elicited ethylene production has also been frequently noted (Knoester et al, 1995;Lasserre et al, 1997) and tobacco mosaic virus-elicited HR lesion formation was delayed in ethylene-insensitive tobacco plants (Knoester et al, 2001). We noted that the kinetics of Psph-elicited HR, as revealed by electrolyte leakage, could be modulated by either adding the C 2 H 4 precursor ACC or the ethylene biosynthesis inhibitor AVG (Fig.…”

Ethylene signaling is required for the acceleration of cell death induced by the activation of AtMEK5 in Arabidopsis

“…The role of ethylene in the pathogenesis of disease and defense responses in infected plants has been studied extensively [28,55]. For example, the onset of HR-like cell death in tobacco infected with TMV [18,56], tomato infected with Cladosporium fulvum [57] and rice infected with Magnaporthe grisea [58] was accompanied by a large burst of ethylene production [59]. Significant suppressed TMV-induced HR-like cell death and expansion was observed in tobacco treated with inhibitors of ethylene biosynthesis or ethylene perception antagonists [56,60].…”

Signaling in Plant Resistance Responses: Divergence and Cross-Talk of Defense Pathways

“…ET plays an important role in senescence (Abeles et al, 1992) and lesion development of hypersensitively reacting plant tissues (Knoester et al, 2001). Since necrotrophic pathogens feed on dead cells, both functions of ET might be favorable for the development of disease caused by such types of pathogens.…”