Viroid Intercellular Trafficking: RNA Motifs, Cellular Factors and Broad Impacts

Abstract

Viroids are noncoding RNAs that infect plants. In order to establish systemic infection, these RNAs must traffic from an initially infected host cell into neighboring cells and ultimately throughout a whole plant. Recent studies have identified structural motifs in a viroid that are required for trafficking, enabling further studies on the mechanisms of their function. Some cellular proteins interact with viroids in vivo and may play a role in viroid trafficking, which can now be directly tested by using a virus-induced gene silencing system that functions efficiently in plant species from which these factors were identified. This review discusses these recent advances, unanswered questions and the use of viroid infection as an highly productive model to elucidate mechanisms of RNA trafficking that is of broad biological significance.

A noncoding plant pathogen provokes both transcriptional and posttranscriptional alterations in tomato

“…Viroids are noncoding pathogens that can infect a broad range of plants causing devastating diseases. How they can regulate the host gene expression through means other than encoding proteins for specific functions still remains unknown . In this sense, the proteomic analysis of viroid‐infected plants constitutes a new promising approach in order to better understand such a host–pathogen relationship.…”

Agents Resembling or Altering Virus Diseases

“…Genetic, structural, and cellular studies on loop 7 (U43/ C318) showed that it is required for PSTVd movement from the bundle sheath into the phloem in N. benthamiana (Zhong et al, 2007;Takeda and Ding, 2009). Structural analysis of this loop region suggested that it might be associated with water insertion, which would distort the local helix, creating a pocket for protein binding.…”

“…In situ hybridization showed presence of PSTVd NB in all cell types, but restriction of PSTVd NT to the phloem and bundle sheath cells of a systemic leaf. (A) From Zhong et al (2008) and (B) from Takeda and Ding (2009) with permission of the publishers. Nucleotide swapping between the two strains showed that four of the 5 nt differences are responsible for the competency of PSTVd NB to move out of bundle sheath cells.…”

“…This indicates the inability of the latter to move from bundle sheath into mesophyll and beyond. Takeda and Ding, 2009) Because viroid intercellular trafficking is mediated by specific structural motifs rather than by diffusion, a simple and generic mechanistic model would predict interactions between these motifs with cellular factors. The four nucleotides (U201, U309, U47/A313) in PSTVdNB strain therefore constitute a so-called bipartite motif that is required for trafficking from the bundle sheath to mesophyll but not Loop 7, which comprises a U/C cis-WC/WC base pair with water insertion and which is required for bundle sheathto-phloem trafficking, is based on Zhong et al (2007).…”

Viroids: Small Probes for Exploring the Vast Universe of RNA Trafficking in Plants

“…Genetic identification of such factors is currently not feasible because all known viroid hosts are not amenable to efficient mutagenesis screening. Biochemical identification of viroid‐interacting proteins, followed by functional studies using targeted gene knockout or knockdown strategies will likely remain a major approach in the perceivable future (Takeda and Ding 2009).…”