Although they are composed only of a small single-stranded circular RNA molecule (300-400 bases) that does not encode any protein, viroids contain enough information to specifically infect their host and modulate genic expression of the plant in their favor, which results in the appearance of certain symptoms ultimately leading to the disease. These properties of viroids, in addition to the presence of a self-catalytic RNA motif within the Avsunviroidae family, support the idea that viroids may have a very ancient origin, which may even be a remnant of an RNA world preceding that of DNA and proteins. This "simplistic" molecule, considered as the boundary of life, seems to be an excellent model for the study of the interactions between pathogens and the cellular machinery of the host and for the study of the evolution of biological molecules.
We used as a model in the laboratory the Peach Latent Mosaic Viroid (PLMVd). Our work is focused on determining the secondary and tertiary structure of this viroid (by mutagenesis, RNases, SHAPE, retention gel, bioinformatics, etc.) to thus discover new motifs within this molecule of RNA that could explain its pathogenicity and its replication. Using the high-throughput sequencing technique, we determined the regions essential for the production of small interfering RNAs following infection with this viroid. This technique also allowed us to understand the evolution of the viroid during an infection and to better characterize the concept of quasi-species.
More recently, using the SHAPE technique, we have been able to determine the secondary structure of all viroids in order to create a compendium of structures. Also, studies on interfering RNAs produced during viroid infection (eg PSTVd), allowed us to identify key genes for the evolution of spindle tuber disease (in potato).
The results of our research will allow a better understanding of the effect of the structure of an RNA pathogen on its infectivity and also its relationship in the mechanism of RNA interference in the plant.