Role of small-RNAs in viroid pathogenesis

Viroids are tiny, circular, naked and infectious RNAs that replicate in the nuclei (family Pospiviroidae) or chloroplasts (family Avsunviroidae) and then invade systemically their host plants, which may react developing severe diseases. Viroid RNAs are targeted by Dicer-like (DCL) ribonucleases generating viroid-derived small RNAs (vd-sRNAs) of 21-24 nt that are loaded into Argonaute (AGO) proteins, the major effectors of RNA silencing. The biological roles of vd-sRNAs have been at least partially unveiled, with data supporting their involvement in anti-viroid defense and pathogenesis. In this respect, it has been shown that symptoms induced by a chloroplast-replicating viroid may be elicited by vd-sRNAs that, resembling structurally and functionally microRNAs, down-regulate the expression of a host gene and trigger pathogenesis via a post-transcriptional RNA silencing-based mechanism. A similar pathogenic mechanism has been proposed for several nuclear-replicating viroids, but the evidence seems less solid. Multidisciplinary approaches, mainly based on genome-wide approaches (degradome sequencing, deep sequencing of vd-sRNAs and transcriptome analyses) should help to clarify whether vd-sRNAs are actually involved in the pathogenesis elicited by nuclear-replicating viroids or alternative molecular mechanisms must be considered.