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

Turnip mosaic virus manipulates DRM2 expression to regulate host CHH and CHG methylation for robust infection.
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芜菁花叶病毒操纵DRM2表达来调节宿主CHH和CHG甲基化以实现强感染

DOI:
10.1007/s44154-022-00052-3
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发表时间:
2022-08-04
期刊:
Stress biology
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其他
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DNA甲基化是一种重要的表观遗传标记,在转座因子(TEs)的抑制和植物免疫调节中起重要作用。然而,人们对RNA病毒如何对抗这种抗病毒机制知之甚少。本研究利用全基因组亚硫酸氢盐测序技术分析了芜菁花叶病毒(TuMV)感染细胞后DNA甲基化的变化。结果表明,TuMV感染细胞后,CHH和CHG的甲基化位点总数增加,其中大部分差异甲基化区域(DMR)与高甲基化相关。基因表达分析表明,在TuMV感染的细胞中,2种甲基化酶(DRM 2和CMT 3)和3种去甲基化酶(ROS 3、DML 2和DML 3)的表达分别显著增加和降低。致病性试验表明,DRM 2功能丧失突变体对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,病毒RNA依赖的RNA聚合酶,能够诱导DRM 2的表达。综上所述,本研究发现TuMV可以通过调控DRM 2的表达来调控宿主DNA甲基化,从而促进病毒感染。在线版本包含补充材料,可通过10.1007/s44154-022-00052-3获取。
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. The online version contains supplementary material available at 10.1007/s44154-022-00052-3.