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烟草对无毒细菌病原体抗性的丧失与水杨酸增强的氧化爆发的减弱有关。

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

作者信息

Mur L A, Brown I R, Darby R M, Bestwick C S, Bi Y M, Mansfield J W, Draper J

机构信息

Institute of Biological Sciences, University of Wales, Aberystwyth, Edward Llwyd Building, Penglais Campus, Aberystwyth, Ceredigion SY23 3DA, UK.

出版信息

Plant J. 2000 Sep;23(5):609-21. doi: 10.1046/j.1365-313x.2000.00825.x.

DOI:10.1046/j.1365-313x.2000.00825.x
PMID:10972887
Abstract

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.

摘要

在野生型烟草品种萨姆逊NN(Samsun NN)叶片以及表达水杨酸羟化酶的转基因株系(35S-SH-L)中,研究了水杨酸(SA)在过敏反应(HR)中细胞死亡前发生的事件里所起的作用。用丁香假单胞菌无毒菌株侵染35S-SH-L烟草,在可见表型、细菌繁殖动力学以及从感染位点逃逸方面,引发了类似于通常与对有毒菌株的亲和性反应相关的症状。与野生型烟草中的反应相比,用无毒细菌侵染35S-SH-L植株后,植物细胞死亡的起始以及活性氧物种响应启动子(AoPR1-GUS)的诱导均延迟。用无毒细菌侵染后发生的氧化爆发通过组织化学方法进行可视化并原位定量。在野生型烟草中,接种后1小时内反应位点处H2O2的积累就很明显,而在35S-SH-L植株中,H2O2积累的起始延迟了2 - 3小时。H2O2产生的延迟与野生型植株接种后1 - 2小时内通常出现的SA短暂升高的降低相关。我们的数据表明,SA早期的短暂升高增强了氧化爆发,从而对H2O2的积累、植物细胞死亡以及防御基因的诱导产生影响,这些因素共同可能决定植物与病原体相互作用的结果。

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