Cytosine methylation is a stable and heritable modification of the DNA that imparts epigenetic control throughout the genome, including regulation of coding and noncoding elements. In plants, previous studies have contributed to shape the epigenetic landscape in developmental processes, whereas the potential for these pathways to be dynamically regulated during non-developmental processes, such as stress responses, has not been investigated thoroughly at date. Recently, it has been demonstrated that DNA methylation is involved in controlling the Arabidopsis thaliana defence response against bacterial pathogens, and several lines of evidence suggest that plant immune response to viral infections imply an involvement of DNA methylation. It has been shown that plant viruses have the capability to modify the methylation profile of the host genome, although with scarce loci-specific methylation. However a high-resolution quantitative analysis of DNA methylation changes, a technology now available for genome-wide investigations (also known as BS-Seq) is still missing in the case of plant-virus interactions. With the aim of investigating how epigenetic mechanisms contribute to the onset and progression of diseases, we used BS-Seq to analyse methylation processes on the host genome induced by a RNA virus (Cucumber mosaic virus, CMV) and a DNA virus (Cauliflower mosaic virus, CaMV). First analysis of the BS-seq data demonstrates that infection of each virus modifies the methylation landscape of all 5 chromosomes. Our data strongly indicate that the mechanism induced by RNA- and DNA-virus infection must be different. Interestingly, the RNA-virus infection mainly induces de-methylation whereas CaMV infection triggers a general hyper-methylation. Investigations on the genomic localization of these modifications result in a similar list of regions affected by the different viruses. On the other side, analysis of the differentially methylated sites according to annotated genes reveals significantly more differentially methylated genes in CMV-than in CaMV-infected plants. Furthermore, gene feature analysis shows prevalent promoter regions de-methylation upon infection of both viruses. However, we find many hypermethylated coding regions in CMV infected plants versus hardly differentially methylated coding regions in DNA-virus infected Arabidopsis. Finally, perhaps the most intriguing concluding remark of this preliminary analysis is that despite we find differentially methylated regions within gene features, such as transcripts, transposon and promoter, the large majority of methylation modifications are located in intergenic (not yet annotated) regions and might cover and regulate still unknown non-coding RNA products.
Differential Arabidopsis genome methylation in response to RNA and DNA virus infection
Carluccio AV;D'Elia D;Cillo F;Gisel A;Stavolone L
2014
Abstract
Cytosine methylation is a stable and heritable modification of the DNA that imparts epigenetic control throughout the genome, including regulation of coding and noncoding elements. In plants, previous studies have contributed to shape the epigenetic landscape in developmental processes, whereas the potential for these pathways to be dynamically regulated during non-developmental processes, such as stress responses, has not been investigated thoroughly at date. Recently, it has been demonstrated that DNA methylation is involved in controlling the Arabidopsis thaliana defence response against bacterial pathogens, and several lines of evidence suggest that plant immune response to viral infections imply an involvement of DNA methylation. It has been shown that plant viruses have the capability to modify the methylation profile of the host genome, although with scarce loci-specific methylation. However a high-resolution quantitative analysis of DNA methylation changes, a technology now available for genome-wide investigations (also known as BS-Seq) is still missing in the case of plant-virus interactions. With the aim of investigating how epigenetic mechanisms contribute to the onset and progression of diseases, we used BS-Seq to analyse methylation processes on the host genome induced by a RNA virus (Cucumber mosaic virus, CMV) and a DNA virus (Cauliflower mosaic virus, CaMV). First analysis of the BS-seq data demonstrates that infection of each virus modifies the methylation landscape of all 5 chromosomes. Our data strongly indicate that the mechanism induced by RNA- and DNA-virus infection must be different. Interestingly, the RNA-virus infection mainly induces de-methylation whereas CaMV infection triggers a general hyper-methylation. Investigations on the genomic localization of these modifications result in a similar list of regions affected by the different viruses. On the other side, analysis of the differentially methylated sites according to annotated genes reveals significantly more differentially methylated genes in CMV-than in CaMV-infected plants. Furthermore, gene feature analysis shows prevalent promoter regions de-methylation upon infection of both viruses. However, we find many hypermethylated coding regions in CMV infected plants versus hardly differentially methylated coding regions in DNA-virus infected Arabidopsis. Finally, perhaps the most intriguing concluding remark of this preliminary analysis is that despite we find differentially methylated regions within gene features, such as transcripts, transposon and promoter, the large majority of methylation modifications are located in intergenic (not yet annotated) regions and might cover and regulate still unknown non-coding RNA products.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
