A loss of resistance to avirulent bacterial pathogens in tobacco is associated with the attenuation of a salicylic acid-potentiated oxidative burst

Awduron Sefydliadau
Math Erthygl
Iaith wreiddiolSaesneg
Tudalennau (o-i)309-621
CyfnodolynPlant Journal
Cyfrol23
Rhif y cyfnodolyn5
Dangosyddion eitem ddigidol (DOIs)
StatwsCyhoeddwyd - 01 Medi 2000
Cysylltiadau
Cysylltiad parhaol
Gweld graff cysylltiadau
Fformatau enwi

Crynodeb

The role of salicylic acid (SA) in events occurring before cell death during the hypersensitive reaction (HR) was investigated in leaves of wild-type tobacco Samsun NN and in transgenic lines expressing salicylate hydroxylase (35S-SH-L). Challenge of 35S-SH-L tobacco with avirulent strains of Pseudomonas syringae gave rise to symptoms resembling those normally associated with a compatible response to virulent strains in terms of visible phenotype, kinetics of bacterial multiplication, and escape from the infection site. Compared with responses in wild-type tobacco, both the onset of plant cell death and the induction of an active oxygen species-responsive promoter (AoPR1-GUS) were delayed following challenge of 35S-SH-L plants with avirulent bacteria. The oxidative burst occurring after challenge with avirulent bacteria was visualized histochemically and quantified in situ. H2O2 accumulation at reaction sites was evident within 1 h after inoculation in wild-type tobacco, whereas in 35S-SH-L plants the onset of H2O2 accumulation was delayed by 2–3 h. The delay in H2O2 generation was correlated with a reduction in the transient rise in SA that usually occurred within 1–2 h following inoculation in wild-type plants. Our data indicate that an early transient rise in SA potentiates the oxidative burst, with resultant effects on accumulation of H2O2, plant cell death and also defence-gene induction, factors that together may determine the outcome of plant–pathogen interactions

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