Résumé
To protect genome integrity against invasive nucleic acids, most eukaryotic organisms have evolved gene silencing mechanisms, often involving small interfering RNAs (siRNAs). Endogenous banana streak virus (eBSV) integrants derived from three distinct species, present in Musa balbisiana (B) but not Musa acuminata (A) banana genomes are able to reconstitute functional episomal viruses in interspecific triploid AAB banana hybrids, causing banana streak disease. In contrast, the seedy diploid (BB) parent line, which harbours identical eBSV loci, does not develop disease. Illumina sequencing revealed that eBSV loci produce low-abundance transcripts covering most of the viral sequence and generate predominantly 24-nt siRNAs, in contrast to predominantly 21–22 nt viral siRNAs derived from the respective episomal viruses in M. acuminata or AAB hybrid plants. Remarkably, siRNA production is restricted to duplicated and inverted viral sequences present in eBSV loci. Using bisulfite sequencing we found that both siRNA-producing and non-producing sequences in the eBSV loci are methylated at 100 % symmetric CG and CHG sites and up to 50% in non-symmetric CHH sites unlike episomal virus DNA previously found to be largely unmethylated. Our data suggest that eBSVs are controlled at the epigenetic level in the BB diploids. This regulation prevents both their awakening and systemic infection of the plant, but probably also serves to confer the resistant phenotype observed in BB plants against mealybug-transmitted viral particles. These findings are thus of relevance to other plant resources hosting integrated viruses.