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

被引:69
作者
Mur, LAJ
Brown, IR
Darby, RM
Bestwick, CS
Bi, YM
Mansfield, JW
Draper, J
机构
[1] Univ Wales, Inst Biol Sci, Aberystwyth SY23 3DA, Dyfed, Wales
[2] Univ London, Wye Coll, Dept Biol Sci, Ashford TN24 5AH, Kent, England
关键词
salicylic acid; potentiation; oxidative burst;
D O I
10.1046/j.1365-313x.2000.00825.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:609 / 621
页数:13
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