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植保素生成缺陷导致拟南芥对真菌链格孢菌的易感性增强。

Deficiency in phytoalexin production causes enhanced susceptibility of Arabidopsis thaliana to the fungus Alternaria brassicicola.

作者信息

Thomma B P, Nelissen I, Eggermont K, Broekaert W F

机构信息

F.A. Janssens Laboratory of Genetics, Katholieke Universiteit Leuven, Heverlee-Leuven, Belgium.

出版信息

Plant J. 1999 Jul;19(2):163-71. doi: 10.1046/j.1365-313x.1999.00513.x.

Abstract

The phytoalexin-deficient Arabidopsis mutant pad3-1, which is affected in the production of the indole-type phytoalexin camalexin, has previously been shown not to display altered susceptibility to either the bacterium Pseudomonas syringae (Glazebrook & Ausubel 1994; Proc. Natl. Acad. Sci. USA, 91: 8955-8959) or the biotrophic fungi Peronospora parasitica (Glazebrook et al. 1997; Genetics, 146: 381-392) and Erysiphe orontii (Reuber et al. 1998; Plant J. 16: 473-485). We now show that this mutant is markedly more susceptible than its wild-type parental line to infection by the necrotrophic fungus Alternaria brassicicola, but not to Botrytis cinerea. A strong camalexin response was elicited in wild-type plants inoculated with either Alternaria brassicicola or Botrytis cinerea, whereas no camalexin could be detected in pad3-1 challenged with these fungi. Hence, PAD3 appears to be a key determinant in resistance to at least A. brassicicola. The induction of salicylate-dependent and jasmonate/ethylene-dependent defense genes was not reduced in Alternaria-challenged pad3-1 plants compared to similarly treated wild-type plants. Camalexin production could not be triggered by exogenous application of either salicylate, ethylene or jasmonate and was not, or not strongly, reduced in mutants with defects in perception of these defense-related signal molecules. Camalexin-production appears to be controlled by a pathway that exhibits little cross-talk with salicylate-, ethylene- and jasmonate-dependent signalling events.

摘要

缺乏植保素的拟南芥突变体pad3 - 1在吲哚型植保素camalexin的产生上存在缺陷,先前的研究表明,它对丁香假单胞菌(Glazebrook和Ausubel,1994年;《美国国家科学院院刊》,91: 8955 - 8959)、活体营养型真菌寄生霜霉(Glazebrook等人,1997年;《遗传学》,146: 381 - 392)和瓜类白粉菌(Reuber等人,1998年;《植物杂志》,16: 473 - 485)的易感性并未改变。我们现在表明,该突变体比其野生型亲本系对坏死营养型真菌链格孢的感染更为敏感,但对灰葡萄孢不敏感。用链格孢或灰葡萄孢接种野生型植物时会引发强烈的camalexin反应,而在用这些真菌攻击的pad3 - 1中未检测到camalexin。因此,PAD3似乎是对至少链格孢抗性的关键决定因素。与同样处理的野生型植物相比,在受到链格孢攻击的pad3 - 1植物中,水杨酸依赖性和茉莉酸/乙烯依赖性防御基因的诱导并未降低。外源施用水杨酸、乙烯或茉莉酸均不能触发camalexin的产生,并且在这些防御相关信号分子感知存在缺陷的突变体中,camalexin的产生并未或未强烈减少。Camalexin的产生似乎受一条与水杨酸、乙烯和茉莉酸依赖性信号事件几乎没有相互作用的途径控制。

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