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芜菁花叶病毒操纵DRM2表达以调节宿主CHH和CHG甲基化,从而实现高效感染。

Turnip mosaic virus manipulates DRM2 expression to regulate host CHH and CHG methylation for robust infection.

作者信息

Wu Xiaoyun, Chai Mengzhu, Liu Jiahui, Jiang Xue, Yang Yingshuai, Guo Yushuang, Li Yong, Cheng Xiaofei

机构信息

Key Laboratory of Germplasm Enhancement, Physiology and Ecology of Food Crops in Cold Region of Chinese Education Ministry, College of Agriculture, Northeast Agricultural University, Harbin, 150030, Heilongjiang, China.

Key Laboratory of Molecular Genetics, Guizhou Academy of Tobacco Science, Guiyang, 550081, China.

出版信息

Stress Biol. 2022 Aug 4;2(1):29. doi: 10.1007/s44154-022-00052-3.

Abstract

DNA methylation is an important epigenetic marker for the suppression of transposable elements (TEs) and the regulation of plant immunity. However, little is known how RNA viruses counter defense such antiviral machinery. In this study, the change of DNA methylation in turnip mosaic virus (TuMV)-infected cells was analyzed by whole genome bisulfite sequencing. Results showed that the total number of methylated sites of CHH and CHG increased in TuMV-infected cells, the majority of differentially methylated regions (DMRs) in the CHH and CHG contexts were associated with hypermethylation. Gene expression analysis showed that the expression of two methylases (DRM2 and CMT3) and three demethylases (ROS3, DML2, DML3) was significantly increased and decreased in TuMV-infected cells, respectively. Pathogenicity tests showed that the enhanced resistance to TuMV of the loss-of-function mutant of DRM2 is associated with unregulated expression of several defense-related genes. Finally, we found TuMV-encoded NIb, the viral RNA-dependent RNA polymerase, was able to induce the expression of DRM2. In conclusion, this study discovered that TuMV can modulate host DNA methylation by regulating the expression of DRM2 to promote virus infection.

摘要

DNA甲基化是抑制转座元件(TEs)和调节植物免疫的重要表观遗传标记。然而,关于RNA病毒如何对抗这种抗病毒机制的了解甚少。在本研究中,通过全基因组亚硫酸氢盐测序分析了芜菁花叶病毒(TuMV)感染细胞中DNA甲基化的变化。结果表明,TuMV感染细胞中CHH和CHG甲基化位点的总数增加,CHH和CHG背景下的大多数差异甲基化区域(DMRs)与高甲基化相关。基因表达分析表明,TuMV感染细胞中两种甲基转移酶(DRM2和CMT3)和三种去甲基化酶(ROS3、DML2、DML3)的表达分别显著增加和减少。致病性测试表明,DRM2功能缺失突变体对TuMV的抗性增强与几个防御相关基因的表达失调有关。最后,我们发现TuMV编码的NIb,即病毒RNA依赖性RNA聚合酶,能够诱导DRM2的表达。总之,本研究发现TuMV可以通过调节DRM2的表达来调节宿主DNA甲基化,从而促进病毒感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da89/10441925/200c51e0f413/44154_2022_52_Fig1_HTML.jpg

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