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Current overview on viroid–host interactions

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Abstract Viroids are one of the most enigmatic highly structured, circular, single‐stranded RNA phytopathogens. Although they are not known to code for any peptide, viroids induce visible symptoms in susceptible host plants that resemble those associated with many plant viruses. It is known that viroids induce disease symptoms by direct interaction with host factors; however, the precise mechanism by which this occurs remains poorly understood. Studies on the host's responses to viroid infection, host susceptibility and nonhost resistance have been underway for several years, but much remains to be done in order to fully understand the complex nature of viroid–host interactions. Recent progress using molecular biology techniques combined with computational algorithms, in particular evidence of the role of viroid‐derived small RNAs in the RNA silencing pathways of a disease network, has widened the knowledge of viroid pathogenicity. The complexity of viroid–host interactions has been revealed in the past decades to include, but not be limited to, the involvement of host factors, viroid structural complexity, and viroid‐induced ribosomal stress, which is further boosted by the discovery of long noncoding RNAs (lncRNAs). In this review, the current understanding of the viroid–host interaction has been summarized with the goal of simplifying the complexity of viroid biology for future research. This article is categorized under: RNA in Disease and Development > RNA in Disease
The most stable secondary structures of potato spindle tuber viroid (PSTVd) and peach latent mosaic viroid (PLMVd). The final structural models of PSTVd (a) and both the (+) and (−) polarities of PLMVd (b) as obtained by inputting the selective 2'‐hydroxyl acylation analyzed by primer extension (SHAPE) data into the RNAstructure software. The nucleotides in black denote those of low SHAPE reactivities (0–0.40), those in orange are of intermediate reactivities (0.40–0.85) and those in red are highly reactive (.0.85). The different structural/functional motifs are delimited by full lines, and the presence of both the A‐motif and the loop E are noted on the PSTVd structure. The nucleotides in the box denote the virulence‐modulating region (VMR). The insertions (red arrows), deletions (green arrows) and substitutions (black arrows) of the nucleotides that are known to determine disease severity are shown on the secondary structure of PSTVd. The nucleotides involved in the formation of the hammerhead are underlined in the PLMVd structures, and the cleavage sites are indicated by an arrow. The asterisks in the hammerhead region of (b) denote the nucleotides mutated in order to avoid self‐cleavage during the in vitro SHAPE analysis
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Putative working model for the production of secondary small interfering RNA (siRNA) and viroid‐induced symptoms. The circular viroid molecule, upon infection, replicates in the host plant via a rolling circular mechanism. Due to both the high degree of internal base‐pairing and the nuclear dsRNA intermediate formed during the viroid's replication (Flores et al., ), it induces the host's RNA silencing machinery through the activity of the DICER‐like (DCL) RNase III‐type ribonucleases, and results in the production of siRNAs called viroid‐derived sRNA (vd‐sRNA). The RNA‐induced silencing complex recruits these vd‐sRNAs in order to direct the degradation of complementary RNAs. This results in the accumulation of aberrant host mRNAs which lack either the 5'‐cap or the 3'‐poly(A)‐tail. These aberrant mRNAs might act as the templates for RDR6 in the presence of SGS3, resulting in the production of dsRNA. This phased production of host dsRNA serves as a substrate for RNA silencing through the DCL4 and DRB4 complexes. This results in the production of several secondary siRNAs that are complementary to the host's RNA, and the cycle thus continues. In a nutshell, the RNA silencing initiated by the viroid is multiplexed by the host's RDR6 to act on the host's own mRNAs, resulting in symptom expression
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Motifs of the members of the Avsunviroidae family involved in pathogenesis. The final structural motifs of the (+) polarities of chrysanthemum chlorotic mottle viroid (CChMVd) (a), the (+) polarity of peach latent mosaic viroid (PLMVd) PC‐C40 (b) and the (+) polarity of avocado sunblotch viroid (ASBVd) (c) were predicted using the mfold web tool (Zuker, ). The nucleotides that are involved in the pathogenesis are shown in the boxes. In (a) the change in the tetraloop nucleotide sequence from GAAA to UUUC converts a latent variant of CChMVd to a severe symptomatic CChMVd one on susceptible chrysanthemum cultivars. In (b) the presence of a 12‐nt hairpin in PLMVd induces the calico effect (bleaching of leaves) in susceptible peach cultivars. In (c) the addition of a U between the bases located at positions 115 and 118 is associated with leaf variegation and bleaching in ASBVd infected avocado plants
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