Epigenetic Changes in Host Ribosomal DNA Promoter Induced by an Asymptomatic Plant Virus Infection
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https://riunet.upv.es/handle/10251/166140
Cita bibliográfica
Pérez-Cañamás, M.; Hevia, E.; Hernandez Fort, C. (2020). Epigenetic Changes in Host Ribosomal DNA Promoter Induced by an Asymptomatic Plant Virus Infection. Biology. 9(5):1-13. https://doi.org/10.3390/biology9050091
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[EN] DNA cytosine methylation is one of the main epigenetic mechanisms in higher eukaryotes
and is considered to play a key role in transcriptional gene silencing. In plants, cytosine methylation can
occur in all sequence contexts (CG, CHG, and CHH), and its levels are controlled by multiple pathways,
including de novo methylation, maintenance methylation, and demethylation. Modulation of DNA
methylation represents a potentially robust mechanism to adjust gene expression following exposure
to different stresses. However, the potential involvement of epigenetics in plant-virus interactions
has been scarcely explored, especially with regard to RNA viruses. Here, we studied the impact of a
symptomless viral infection on the epigenetic status of the host genome. We focused our attention
on the interaction between Nicotiana benthamiana and Pelargonium line pattern virus (PLPV, family
Tombusviridae), and analyzed cytosine methylation in the repetitive genomic element corresponding to
ribosomal DNA (rDNA). Through a combination of bisulfite sequencing and RT-qPCR, we obtained
data showing that PLPV infection gives rise to a reduction in methylation at CG sites of the rDNA
promoter. Such a reduction correlated with an increase and decrease, respectively, in the expression
levels of some key demethylases and of MET1, the DNA methyltransferase responsible for the
maintenance of CG methylation. Hypomethylation of rDNA promoter was associated with a
five-fold augmentation of rRNA precursor levels. The PLPV protein p37, reported as a suppressor of
post-transcriptional gene silencing, did not lead to the same effects when expressed alone and, thus,
it is unlikely to act as suppressor of transcriptional gene silencing. Collectively, the results suggest
that PLPV infection as a whole is able to modulate host transcriptional activity through changes in the
cytosine methylation pattern arising from misregulation of methyltransferases/demethylases balance.
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Biology