首页> 外文期刊>Plant physiology >Ethylene Modulates the Role of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 in Cross Talk between Salicylate and Jasmonate Signaling
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Ethylene Modulates the Role of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 in Cross Talk between Salicylate and Jasmonate Signaling

机译:乙烯在水杨酸和茉莉酸信号之间的串扰中调节与发病相关的基因1的非表达子的作用。

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摘要

The plant hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) play crucial roles in the signaling network that regulates induced defense responses against biotic stresses. Antagonism between SA and JA operates as a mechanism to fine-tune defenses that are activated in response to multiple attackers. In Arabidopsis (Arabidopsis thaliana), NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) was demonstrated to be required for SA-mediated suppression of JA-dependent defenses. Because ET is known to enhance SA/NPR1-dependent defense responses, we investigated the role of ET in the SA-JA signal interaction. Pharmacological experiments with gaseous ET and the ET precursor 1-aminocyclopropane-1-carboxylic acid showed that ET potentiated SA/NPR1-dependent PATHOGENESIS-RELATED1 transcription, while it rendered the antagonistic effect of SA on methyl jasmonate-induced PDF1.2 and VSP2 expression NPR1 independent. This overriding effect of ET on NPR1 function in SA-JA cross talk was absent in the npr1-1/ein2-1 double mutant, demonstrating that it is mediated via ET signaling. Abiotic and biotic induction of the ET response similarly abolished the NPR1 dependency of the SA-JA signal interaction. Furthermore, JA-dependent resistance against biotic attackers was antagonized by SA in an NPR1-dependent fashion only when the plant-attacker combination did not result in the production of high levels of endogenous ET. Hence, the interaction between ET and NPR1 plays an important modulating role in the fine tuning of the defense signaling network that is activated upon pathogen and insect attack. Our results suggest a model in which ET modulates the NPR1 dependency of SAJA antagonism, possibly to compensate for enhanced allocation of NPR1 to function in SA-dependent activation of PR genes.
机译:植物激素水杨酸(SA),茉莉酸(JA)和乙烯(ET)在调节诱导的抵抗生物胁迫的防御信号的信号网络中起着关键作用。 SA和JA之间的对抗是一种机制,用于微调针对多个攻击者而激活的防御。在拟南芥(Arabidopsis thaliana)中,已证明,与SA介导的JA依赖性防御相关的非光生病相关基因1(NPR1)的非表达子。因为已知ET可以增强SA / NPR1依赖性防御反应,所以我们研究了ET在SA-JA信号相互作用中的作用。用气态ET和ET前体1-氨基环丙烷-1-羧酸进行的药理实验表明,ET增强了SA / NPR1依赖的PATHOGENESIS-RELATED1转录,同时赋予SA对茉莉酸甲酯诱导的PDF1.2和VSP2表达的拮抗作用。 NPR1独立。 ET对SA-JA串扰中NPR1功能的这种压倒性作用在npr1-1 / ein2-1双重突变体中不存在,表明它是通过ET信号传导介导的。 ET反应的非生物和生物诱导同样消除了SA-JA信号相互作用的NPR1依赖性。此外,仅当植物-攻击者组合未产生高水平的内源性ET时,SA才会以NPR1依赖性拮抗JA对生物攻击者的抗性。因此,ET和NPR1之间的相互作用在防御信号网络的微调中起着重要的调节作用,该防御信号网络在病原体和昆虫侵袭时被激活。我们的结果提出了一个模型,其中ET调节SAJA拮抗作用的NPR1依赖性,可能是为了补偿NPR1的增强分配,以发挥SA依赖性PR基因的激活作用。

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