Hijack to escape: a geminivirus seizes a host imprinted E3 ligase to escape epigenetic repression
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jack to escape: a geminivirus seizes a host imprinted E3 ligase to escape epigenetic repression 1,2*
Xueping Zhou 1
State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, 2
Beijing 100193, China; State Key Laboratory of Rice Biology, Institute of Biotechnology, Zhejiang University, Hangzhou 310058, China Received September 14, 2020; accepted October 9, 2020; published online October 19, 2020
Citation:
Zhou, X. (2020). Hijack to escape: a geminivirus seizes a host imprinted E3 ligase to escape epigenetic repression. Sci China Life Sci 63, https://doi. org/10.1007/s11427-020-1829-4
Geminivirus infection triggers both transcriptional and posttranscriptional RNA silencing (RNA interference, RNAi) antiviral mechanisms. Much is known about the geminivirus-encoded viral suppressors of RNA silencing (VSRs) interfering with host RNAi machineries. However, how transcription of these VSRs escapes from epigenetic silencing remains unknown. Chen et al. (2020) provide compelling evidence for the epigenetic activation of VSRs via geminivirus-induced VIM5, a plant imprinted E3 ligase gene, leading to post-translational degradation of host DNA methyltransferases (Chen et al., 2020). Geminiviruses belong to one of the largest families of plant viruses, with genomes comprising one or two single-stranded circular DNAs. Geminiviruses infect many economically important crops, causing devastating diseases and leading to considerable yield losses worldwide (Rojas et al., 2005; Yang et al., 2019). The plant hosts have evolved antiviral immunity such as RNA silencing, which includes post-transcriptional gene silencing (PTGS) of viral transcripts and transcriptional gene silencing (TGS) of the viral DNA. Geminiviruses cannot afford to encode many proteins to complete their infection cycle. Thus, most of the geminiviral proteins, including Rep, C2, C4, and V2, efficiently affect several host developmental and hormonal pathways to overcome both TGS and PTGS as viral suppressors of RNA silencing (VSRs) (Zhang et al., 2011; Rodríguez-Negrete et *Corresponding author (email: [email protected])
al., 2013; Yang et al., 2013; Mei et al., 2018; Wang et al., 2018; Mei et al., 2020). DNA methylation at the 5′-position of cytosine in epigenetic regulation and genome stability is well-characterized (Zhang et al., 2018). In Arabidopsis, the maintenance of cytosine methylation in the CG and CHG contexts is performed by DNA methyltransferases MET1and CMT3, respectively, whereas DRM2 catalyzes de novo DNA methylation in all CG, CHG, and CHH contexts. Multiple DNA methylation-associated Arabidopsis mutants exhibit dramatically more severe symptoms than the wild-type plants when infected with geminiviruses (Raja et al., 2008). Further evidence supporting epigenetic anti-geminiviral silencing came from the functions of geminiviral VSRs. Infection with several begomoviruses or with the cutovirus Beet curly top virus (BCTV) reduced the mRNA levels of both MET1 and CMT3, but
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