Reactive electrophile species activate defense gene expression in Arabidopsis

Reactive electrophile species activate defense gene expression in Arabidopsis
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DOI:
10.1046/j.1365-313x.2003.01718.x
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发表时间:
2003-04-01
期刊:
影响因子:
7.2
通讯作者:
Farmer, EE
Farmer, EE
中科院分区:
生物学1区
文献类型:
--
作者:
Alméras, E;Stolz, S;Farmer, EE

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含有α,β-不饱和羰基的化合物越来越多地被认为是基因表达的有效调节者;一些是已知的强大的细胞毒素,在宿主-病原体相互作用的病变形成部位积累。我们使用一种可靠的光合作用效率测量方法来量化各种脂肪衍生物在拟南芥叶片中的毒性。小的α,β不饱和羰基化合物(如丙烯醛和甲基乙烯基酮)具有很高的活性,并被证明是致病相关基因HEL(PR4)表达的有力刺激因子。这些小的挥发性亲电体比2(E)-己烯醛等较大的烯烃同系物活性高得多,并以一种独立于水杨酸盐、乙烯和茉莉酸产生/感受的方式激活HEL的表达。电处理大大增加了未酯化的环戊酮茉莉酸酯的水平,这些茉莉酸酯本身就是亲电性的。比较了对电泳法处理和对无毒细菌的反应的基因表达模式,显示出惊人的相似转录谱。这些结果扩大了反应性电泳菌的已知生物效应的范围,包括对致病相关基因(HEL)和参与新陈代谢的基因的激活。亲电体可以作为核心防御信号转导中的遗传和生化效应的中介。
Compounds containing alpha,beta-unsaturated carbonyl groups are increasingly implicated as potent regulators of gene expression; some are powerful cytotoxins known to accumulate at the site of lesion formation in host-pathogen interactions. We used a robust measurement of photosynthetic efficiency to quantify the toxicity of a variety of lipid derivatives in Arabidopsis leaves. Small alpha,beta-unsaturated carbonyl compounds (e.g. acrolein and methyl vinyl ketone) were highly active and proved to be potent stimulators of expression of the pathogenesis-related gene HEL (PR4). These small volatile electrophiles were far more active than larger alkenal homologs like 2(E)-hexenal, and activated HEL expression in a manner independent of salicylate, ethylene, and jasmonate production/perception. Electrophile treatment massively increased the levels of unesterified cyclopentenone jasmonates, which themselves are electrophiles. Patterns of gene expression in response to electrophile treatment and in response to avirulent bacteria were compared, which revealed strikingly similar transcript profiles. The results broaden the range of known biologic effects of reactive electrophile species to include the activation of a pathogenesis-related gene (HEL) and genes involved in metabolism. Electrophiles can act as mediators of both genetic and biochemical effects on core defense signal transduction.