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拟南芥中植物防御素基因的诱导需要茉莉酸和乙烯反应途径的同时激活。

Concomitant activation of jasmonate and ethylene response pathways is required for induction of a plant defensin gene in Arabidopsis.

作者信息

Penninckx I A, Thomma B P, Buchala A, Métraux J P, Broekaert W F

机构信息

F.A. Janssens Laboratory of Genetics, Katholieke Universiteit Leuven, Kardinaal Mercierlaan 92, B-3001 Heverlee-Leuven, Belgium.

出版信息

Plant Cell. 1998 Dec;10(12):2103-13. doi: 10.1105/tpc.10.12.2103.

Abstract

Activation of the plant defensin gene PDF1.2 in Arabidopsis by pathogens has been shown previously to be blocked in the ethylene response mutant ein2-1 and the jasmonate response mutant coi1-1. In this work, we have further investigated the interactions between the ethylene and jasmonate signal pathways for the induction of this defense response. Inoculation of wild-type Arabidopsis plants with the fungus Alternaria brassicicola led to a marked increase in production of jasmonic acid, and this response was not blocked in the ein2-1 mutant. Likewise, A. brassicicola infection caused stimulated emission of ethylene both in wild-type plants and in coi1-1 mutants. However, treatment of either ein2-1 or coi1-1 mutants with methyl jasmonate or ethylene did not induce PDF1.2, as it did in wild-type plants. We conclude from these experiments that both the ethylene and jasmonate signaling pathways need to be triggered concomitantly, and not sequentially, to activate PDF1.2 upon pathogen infection. In support of this idea, we observed a marked synergy between ethylene and methyl jasmonate for the induction of PDF1.2 in plants grown under sterile conditions. In contrast to the clear interdependence of the ethylene and jasmonate pathways for pathogen-induced activation of PDF1.2, functional ethylene and jasmonate signaling pathways are not required for growth responses induced by jasmonate and ethylene, respectively.

摘要

先前研究表明,在拟南芥中,病原体激活植物防御素基因PDF1.2的过程在乙烯反应突变体ein2-1和茉莉酸反应突变体coi1-1中受阻。在本研究中,我们进一步探究了乙烯和茉莉酸信号通路之间在诱导这种防御反应中的相互作用。用真菌链格孢接种野生型拟南芥植株会导致茉莉酸产量显著增加,且这一反应在ein2-1突变体中并未受阻。同样,链格孢感染在野生型植株和coi1-1突变体中均会引起乙烯的释放增加。然而,用茉莉酸甲酯或乙烯处理ein2-1或coi1-1突变体均不会像在野生型植株中那样诱导PDF1.2。我们从这些实验得出结论,在病原体感染时,乙烯和茉莉酸信号通路都需要同时被触发,而非依次触发,才能激活PDF1.2。支持这一观点的是,我们观察到在无菌条件下生长的植物中,乙烯和茉莉酸甲酯在诱导PDF1.2方面存在显著协同作用。与病原体诱导激活PDF1.2时乙烯和茉莉酸信号通路明显的相互依赖性不同,分别由茉莉酸和乙烯诱导的生长反应并不需要功能性的乙烯和茉莉酸信号通路。

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