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N-3-氧代-辛酰基高丝氨酸内酯介导的拟南芥对丁香假单胞菌抗性的激发需要水杨酸信号通路。

N-3-oxo-octanoyl-homoserine lactone-mediated priming of resistance to Pseudomonas syringae requires the salicylic acid signaling pathway in Arabidopsis thaliana.

机构信息

Biology Institute, Hebei Academy of Sciences, 46th South Street of Friendship, Shijiazhuang, 050051, China.

Hebei Engineering and Technology Center of Microbiological Control on Main Crop Disease, 46th South Street of Friendship, Shijiazhuang, 050051, China.

出版信息

BMC Plant Biol. 2020 Jan 28;20(1):38. doi: 10.1186/s12870-019-2228-6.

DOI:10.1186/s12870-019-2228-6
PMID:31992205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6986161/
Abstract

BACKGROUD

Many Gram-negative bacteria use N-acyl-homoserine lactones (AHLs) to communicate each other and to coordinate their collective behaviors. Recently, accumulating evidence shows that host plants are able to sense and respond to bacterial AHLs. Once primed, plants are in an altered state that enables plant cells to more quickly and/or strongly respond to subsequent pathogen infection or abiotic stress.

RESULTS

In this study, we report that pretreatment with N-3-oxo-octanoyl-homoserine lactone (3OC8-HSL) confers resistance against the pathogenic bacterium Pseudomonas syringae pv. tomato DC3000 (PstDC3000) in Arabidopsis. Pretreatment with 3OC8-HSL and subsequent pathogen invasion triggered an augmented burst of hydrogen peroxide, salicylic acid accumulation, and fortified expression of the pathogenesis-related genes PR1 and PR5. Upon PstDC3000 challenge, plants treated with 3OC8-HSL showed increased activities of defense-related enzymes including peroxidase, catalase, phenylalanine ammonialyase, and superoxide dismutase. In addition, the 3OC8-HSL-primed resistance to PstDC3000 in wild-type plants was impaired in plants expressing the bacterial NahG gene and in the npr1 mutant. Moreover, the expression levels of isochorismate synthases (ICS1), a critical salicylic acid biosynthesis enzyme, and two regulators of its expression, SARD1 and CBP60g, were potentiated by 3OC8-HSL pretreatment followed by pathogen inoculation.

CONCLUSIONS

Our data indicate that 3OC8-HSL primes the Arabidopsis defense response upon hemibiotrophic bacterial infection and that 3OC8-HSL-primed resistance is dependent on the SA signaling pathway. These findings may help establish a novel strategy for the control of plant disease.

摘要

背景

许多革兰氏阴性菌使用 N-酰基高丝氨酸内酯(AHLs)相互交流并协调其集体行为。最近,越来越多的证据表明,宿主植物能够感知和响应细菌 AHLs。一旦被启动,植物就处于一种改变的状态,使植物细胞能够更快和/或更强地对随后的病原体感染或非生物胁迫做出反应。

结果

在这项研究中,我们报告说,用 N-3-氧代-辛酰高丝氨酸内酯(3OC8-HSL)预处理可赋予拟南芥对病原菌丁香假单胞菌 pv.番茄 DC3000(PstDC3000)的抗性。用 3OC8-HSL 预处理和随后的病原体入侵引发了过氧化氢、水杨酸积累的增强爆发,以及与发病相关的基因 PR1 和 PR5 的强化表达。在 PstDC3000 攻击后,用 3OC8-HSL 处理的植物显示出防御相关酶如过氧化物酶、过氧化氢酶、苯丙氨酸氨裂解酶和超氧化物歧化酶的活性增加。此外,在表达细菌 NahG 基因的植物和 npr1 突变体中,3OC8-HSL 预处理对 PstDC3000 的抗性在野生型植物中受损。此外,异分支酸合酶(ICS1)的表达水平,一种关键的水杨酸生物合成酶,以及其表达的两个调节剂 SARD1 和 CBP60g,在 3OC8-HSL 预处理后被增强,随后进行病原体接种。

结论

我们的数据表明,3OC8-HSL 在半生物性细菌感染时启动拟南芥防御反应,3OC8-HSL 诱导的抗性依赖于 SA 信号通路。这些发现可能有助于建立一种控制植物病害的新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/a0e47732e438/12870_2019_2228_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/c37d500fa887/12870_2019_2228_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/aa8ee2065e0f/12870_2019_2228_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/06c7f7ea1e29/12870_2019_2228_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/cd9934d7b087/12870_2019_2228_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/7e269fd9d58b/12870_2019_2228_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/a0e47732e438/12870_2019_2228_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/c37d500fa887/12870_2019_2228_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/aa8ee2065e0f/12870_2019_2228_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/06c7f7ea1e29/12870_2019_2228_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/cd9934d7b087/12870_2019_2228_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/7e269fd9d58b/12870_2019_2228_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a983/6986161/a0e47732e438/12870_2019_2228_Fig6_HTML.jpg

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