A putative antiviral role of plant cytidine deaminases

A mechanism of innate antiviral immunity operating against viruses infecting mammalian cells has been described during the last decade. Host cytidine deaminases ( ., APOBEC3 proteins) edit viral genomes, giving rise to hypermutated nonfunctional viruses; consequently, viral fitness is reduced through lethal mutagenesis. By contrast, sub-lethal hypermutagenesis may contribute to virus evolvability by increasing population diversity. To prevent genome editing, some viruses have evolved proteins that mediate APOBEC3 degradation. The model plant genome encodes nine cytidine deaminases ( CDAs), raising the question of whether deamination is an antiviral mechanism in plants as well. Here we tested the effects of expression of CDAs on the pararetrovirus Cauliflower mosaic virus (CaMV). Two different experiments were carried out. First, we transiently overexpressed each one of the nine genes in plants infected with CaMV, and characterized the resulting mutational spectra, comparing them with those generated under normal conditions. Secondly, we created transgenic plants expressing an artificial microRNA designed to knock-out the expression of up to six genes. This and control plants were then infected with CaMV. Virus accumulation and mutational spectra where characterized in both types of plants. We have shown that the gene product exerts a mutagenic activity, significantly increasing the number of G to A mutations , with a concomitant reduction in the amount of CaMV genomes accumulated. Furthermore, the magnitude of this mutagenic effect on CaMV accumulation is positively correlated with the level of mRNA expression in the plant. Our results suggest that deamination of viral genomes may also work as an antiviral mechanism in plants.