Chassot Céline, Buchala Antony, Schoonbeek Henk-Jan, Métraux Jean-Pierre, Lamotte Olivier
Department of Biology, University of Fribourg, 10 Chemin du Musée, CH-1700 Fribourg, Switzerland.
Plant J. 2008 Aug;55(4):555-67. doi: 10.1111/j.1365-313X.2008.03540.x. Epub 2008 Apr 30.
Physical injury inflicted on living tissue makes it vulnerable to invasion by pathogens. Wounding of Arabidopsis thaliana leaves, however, does not conform to this concept and leads to immunity to Botrytis cinerea, the causal agent of grey mould. In wounded leaves, hyphal growth was strongly inhibited compared to unwounded controls. Wound-induced resistance was not associated with salicylic acid-, jasmonic acid- or ethylene-dependent defence responses. The phytoalexin camalexin was found to be involved in this defence response as camalexin-deficient mutants were not protected after wounding and the B. cinerea strains used here were sensitive to this compound. Wounding alone did not lead to camalexin production but primed its accumulation after inoculation with B. cinerea, further supporting the role of camalexin in wound-induced resistance. In parallel with increased camalexin production, genes involved in the biosynthesis of camalexin were induced faster in wounded and infected plants in comparison with unwounded and infected plants. Glutathione was also found to be required for resistance, as mutants deficient in gamma-glutamylcysteine synthetase showed susceptibility to B. cinerea after wounding, indicating that wild-type basal levels of glutathione are required for the wound-induced resistance. Furthermore, expression of the gene encoding glutathione-S-transferase 1 was primed by wounding in leaves inoculated with B. cinerea. In addition, the priming of MAP kinase activity was observed after inoculation of wounded leaves with B. cinerea compared to unwounded inoculated controls. Our results demonstrate how abiotic stress can induce immunity to virulent strains of B. cinerea, a process that involves camalexin and glutathione.
对活组织造成的物理损伤会使其易受病原体入侵。然而,拟南芥叶片受伤并不符合这一概念,反而会导致对灰霉病(灰霉病的致病因子)产生免疫。与未受伤的对照相比,受伤叶片中的菌丝生长受到强烈抑制。伤口诱导的抗性与水杨酸、茉莉酸或乙烯依赖性防御反应无关。发现植物抗毒素camalexin参与了这种防御反应,因为camalexin缺陷型突变体在受伤后没有受到保护,并且这里使用的灰葡萄孢菌株对这种化合物敏感。单独的伤口不会导致camalexin的产生,但在接种灰葡萄孢后会引发其积累,进一步支持了camalexin在伤口诱导抗性中的作用。与camalexin产量增加同时,与camalexin生物合成相关的基因在受伤和感染的植物中比未受伤和感染的植物中诱导得更快。还发现谷胱甘肽是抗性所必需的,因为缺乏γ-谷氨酰半胱氨酸合成酶的突变体在受伤后对灰葡萄孢敏感,这表明伤口诱导抗性需要野生型谷胱甘肽的基础水平。此外,在接种灰葡萄孢的叶片中,伤口引发了编码谷胱甘肽-S-转移酶1的基因的表达。此外,与未受伤接种的对照相比,在受伤叶片接种灰葡萄孢后观察到促分裂原活化蛋白激酶活性的引发。我们的结果证明了非生物胁迫如何诱导对灰葡萄孢强毒株的免疫,这一过程涉及camalexin和谷胱甘肽。