Viroids are the smallest known infectious agents and induce disease in a wide variety of plant hosts, including many crop species. Ranging in size from ca. 250–400 nucleotides (nt) replication of their single-stranded, circular, non-coding RNA genomes is entirely dependent on transcriptional and processing machinery supplied by the host. Their small size and unique molecular structure makes these molecules an attractive system with which to analyze many different aspects of host–pathogen interaction.
Although replication occurs in different subcellular compartments, members of both families of viroids induce RNA silencing and the accumulation of viroid-specific small RNAs following infection. Post-transcriptional gene silencing (RNA silencing) provides a multi-layer defense system which protects plants from invasion by exogenous RNA replicons such as viruses and viroids. Silencing is triggered by conversion of double-stranded or hairpin RNAs to small RNAs whose sizes ranging between 18 and 26 nucleotides. Infected plants contain high levels of viroid-specific small RNAs, but the circular genomic RNAs themselves appear relatively resistant to RNA silencing – raising the possibility that viroid replication may also be resistant. The mechanism underlying this resistance/tolerance is not yet understood, but certain transgenic tomato lines expressing high levels of hairpin RNA-derived small viroid RNAs are resistant to infection. This paper looks at the accumulation pattern and size distribution of viroid-specific small RNAs in infected plants and identifies several potential targets for RNA silencing mediated by small RNAs.
Accumulation of Potato spindle tuber viroid-specific small RNAs is accompanied by specific changes in gene expression in two tomato cultivars. Virology. 24 Feb 2011
To better understand the biogenesis of viroid-specific small RNAs and their possible role in disease induction, we have examined the accumulation of these small RNAs in potato spindle tuber viroid (PSTVd)-infected tomato plants. Large-scale sequence analysis of viroid-specific small RNAs revealed active production from the upper portion of the pathogenicity and central domains, two regions previously thought to be underrepresented. Profiles of small RNA populations derived from PSTVd antigenomic RNA were more variable, with differences between infected Rutgers (severe symptoms) and Moneymaker (mild symptoms) plants pointing to possible cultivar-specific differences in small RNA synthesis and/or stability. Using microarray analysis, we monitored the effects of PSTVd infection on the expression levels of >100 tomato genes containing potential binding sites for PSTVd small RNAs. Of 18 such genes down-regulated early in infection, two genes involved in gibberellin or jasmonic acid biosynthesis contain binding sites for PSTVd small RNAs in their respective ORFs.