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Updated: Jul 17, 2025

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Turnip mosaic virus manipulates DRM2 expression to regulate host CHH and CHG methylation for robust infection
Xiaoyun Wu1, Mengzhu Chai1, Jiahui Liu1
1Key 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.
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.

