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桃蚜诱导的脂肪酶 1 和茉莉酸的拮抗作用影响拟南芥-禾谷镰刀菌互作的结果。

Opposing effects of MYZUS PERSICAE-INDUCED LIPASE 1 and jasmonic acid influence the outcome of Arabidopsis thaliana-Fusarium graminearum interaction.

机构信息

Department of Biological Sciences, University of North Texas, Denton, Texas, USA.

BioDiscovery Institute, University of North Texas, Denton, Texas, USA.

出版信息

Mol Plant Pathol. 2022 Aug;23(8):1141-1153. doi: 10.1111/mpp.13216. Epub 2022 Apr 9.

DOI:10.1111/mpp.13216
PMID:35396792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9276950/
Abstract

Fusarium graminearum (Fg) is an important fungal pathogen of small grain cereals that can also infect Arabidopsis thaliana. In Arabidopsis, jasmonic acid (JA) signalling involving JASMONATE RESISTANT 1 (JAR1), which synthesizes JA-isoleucine, a signalling form of JA, promotes susceptibility to Fg. Here we show that Arabidopsis MYZUS PERSICAE-INDUCED LIPASE 1 (MPL1), via its influence on limiting JA accumulation, restricts Fg infection. MPL1 expression was up-regulated in response to Fg infection, and MPL1-OE plants, which overexpress MPL1, exhibited enhanced resistance against Fg. In comparison, disease severity was higher on the mpl1 mutant than the wild type. JA content was lower in MPL1-OE and higher in mpl1 than in the wild type, indicating that MPL1 limits JA accumulation. Pharmacological experiments confirmed the importance of MPL1-determined restriction of JA accumulation on curtailment of Fg infection. Methyl-JA application attenuated the MPL1-OE-conferred resistance, while the JA biosynthesis inhibitor ibuprofen enhanced resistance in mpl1. Also, the JA biosynthesis-defective opr3 mutant was epistatic to mpl1, resulting in enhanced resistance in mpl1 opr3 plants. In comparison, JAR1 was not essential for the mpl1-conferred susceptibility to Fg. Considering that methyl-JA promotes Fg growth in culture, we suggest that in part MPL1 curtails disease by limiting the availability of a plant-derived Fg growth-promoting factor.

摘要

镰刀菌禾谷种(Fg)是一种重要的小谷物真菌病原体,也可以感染拟南芥。在拟南芥中,茉莉酸(JA)信号转导涉及茉莉酸抗性 1(JAR1),它合成 JA-异亮氨酸,JA 的信号形式,促进对 Fg 的易感性。在这里,我们表明,拟南芥桃蚜诱导的脂肪酶 1(MPL1)通过其对限制 JA 积累的影响,限制 Fg 感染。MPL1 的表达响应 Fg 感染而上调,并且过表达 MPL1 的 MPL1-OE 植物对 Fg 表现出增强的抗性。相比之下,mpl1 突变体上的疾病严重程度高于野生型。MPL1-OE 和 mpl1 中的 JA 含量低于野生型,表明 MPL1 限制 JA 积累。药理学实验证实了 MPL1 决定的 JA 积累限制对减少 Fg 感染的重要性。甲基-JA 的应用减弱了 MPL1-OE 赋予的抗性,而 JA 生物合成抑制剂布洛芬增强了 mpl1 的抗性。此外,JA 生物合成缺陷型 opr3 突变体与 mpl1 上位性,导致 mpl1 opr3 植物的抗性增强。相比之下,JAR1 对 mpl1 赋予的对 Fg 的易感性不是必需的。考虑到甲基-JA 在培养中促进 Fg 的生长,我们认为 MPL1 部分通过限制植物来源的 Fg 生长促进因子的可用性来限制疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/ff2b8ce4d828/MPP-23-1141-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/46827049b321/MPP-23-1141-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/68768c8b2a3b/MPP-23-1141-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/bbf0f83b6c87/MPP-23-1141-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/938fb15fc02c/MPP-23-1141-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/345ed8a978de/MPP-23-1141-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/ff2b8ce4d828/MPP-23-1141-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/46827049b321/MPP-23-1141-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/68768c8b2a3b/MPP-23-1141-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/bbf0f83b6c87/MPP-23-1141-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/938fb15fc02c/MPP-23-1141-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/345ed8a978de/MPP-23-1141-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/742d/9276950/ff2b8ce4d828/MPP-23-1141-g005.jpg

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