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三羧酸酯诱导对……中细菌的防御预激发

Tricarboxylates Induce Defense Priming Against Bacteria in .

作者信息

Balmer Andrea, Pastor Victoria, Glauser Gaetan, Mauch-Mani Brigitte

机构信息

Laboratory of Molecular and Cell Biology, Institute of Biology, University of Neuchâtel, Neuchâtel, Switzerland.

Metabolic Integration and Cell Signaling Group, Plant Physiology Section, Department of CAMN, Universitat Jaume I, Castellon, Spain.

出版信息

Front Plant Sci. 2018 Aug 20;9:1221. doi: 10.3389/fpls.2018.01221. eCollection 2018.

DOI:10.3389/fpls.2018.01221
PMID:30177948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6110165/
Abstract

Exposure of plants to biotic stress results in an effective induction of numerous defense mechanisms that involve a vast redistribution within both primary and secondary metabolisms. For instance, an alteration of tricarboxylic acid (TCA) levels can accompany the increase of plant resistance stimulated by various synthetic and natural inducers. Moreover, components of the TCA flux may play a role during the set-up of plant defenses. In this study, we show that citrate and fumarate, two major components of the TCA cycle, are able to induce priming in Arabidopsis against the bacterial pathogen pv. DC3000. Both citrate and fumarate show no direct antimicrobial effect and therefore enhanced bacterial resistance found is solely based on the induction of the plant defense system. During the priming phase, both TCA intermediates did not induce any changes in transcript abundances of a set of defense genes, and in phytohormones and camalexin levels. However, at early time points of bacterial challenge, citrate induced a stronger salicylic acid and camalexin accumulation followed later by a boost of the jasmonic acid pathway. On the other hand, adaptations of hormonal pathways in fumarate-treated plants were more complex. While jasmonic acid was not induced, mutants impaired in jasmonic acid perception failed to mount a proper priming response induced by fumarate. Our results suggest that changes in carboxylic acid abundances can enhance Arabidopsis defense through complex signaling pathways. This highlights a promising feature of TCAs as novel defense priming agents and calls for further exploration in other pathosystems and stress situations.

摘要

植物暴露于生物胁迫下会有效诱导多种防御机制,这涉及到初级和次级代谢的大量重新分配。例如,三羧酸(TCA)水平的改变可能伴随着各种合成和天然诱导剂刺激植物抗性的增加。此外,TCA通量的组成部分可能在植物防御的建立过程中发挥作用。在本研究中,我们表明柠檬酸和富马酸,TCA循环的两个主要成分,能够诱导拟南芥对细菌病原体丁香假单胞菌番茄致病变种pv. DC3000产生免疫启动。柠檬酸和富马酸均无直接抗菌作用,因此所发现的增强的细菌抗性完全基于植物防御系统的诱导。在免疫启动阶段,这两种TCA中间产物均未诱导一组防御基因的转录丰度、植物激素和茉莉酸水平发生任何变化。然而,在细菌攻击的早期时间点,柠檬酸诱导了更强的水杨酸和茉莉酸积累,随后茉莉酸途径得到增强。另一方面,富马酸处理植物中激素途径的适应性更为复杂。虽然未诱导茉莉酸,但茉莉酸感知受损的突变体未能对富马酸诱导的免疫启动反应做出适当反应。我们的结果表明,羧酸丰度的变化可以通过复杂的信号通路增强拟南芥的防御。这突出了TCA作为新型防御启动剂的一个有前景的特性,并呼吁在其他病理系统和胁迫情况下进行进一步探索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/f4ec42007808/fpls-09-01221-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/f91a0f6f614d/fpls-09-01221-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/bdd92f1f5273/fpls-09-01221-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/56e06b04f85e/fpls-09-01221-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/73235b5f5b24/fpls-09-01221-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/0d0c8ac36ab1/fpls-09-01221-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/baeb629eed06/fpls-09-01221-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/fca248ba4f23/fpls-09-01221-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/f4ec42007808/fpls-09-01221-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/f91a0f6f614d/fpls-09-01221-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/bdd92f1f5273/fpls-09-01221-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/56e06b04f85e/fpls-09-01221-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/73235b5f5b24/fpls-09-01221-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/0d0c8ac36ab1/fpls-09-01221-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/baeb629eed06/fpls-09-01221-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/fca248ba4f23/fpls-09-01221-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd7f/6110165/f4ec42007808/fpls-09-01221-g008.jpg

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