Roossinck Lab
Research
- We are interested in virus evolution and ecology in host disease and health. We use plant and fungal viruses as model systems. The fundamental questions we are addressing are:
- How and why would a virus become a pathogen?
- What is the role of viruses in natural systems?
- What are the molecular mechanisms of virus evolution?
Our model viruses: We use Cucumber mosaic virus (CMV) as a model for many of our studies (Roossinck, 2001). CMV is a species in the genus Cucumovirus and the family Bromoviridae. CMV is a plus-sense RNA virus with a divided genome. It infects about 1200 species of plants, which is the broadest host range of any known virus. RNA 1 (about 3400 nt) encodes the 1a protein that is involved in replication and has the motifs of a methyl transferase (presumed to provide the 5' cap structure to the genomic RNAs) and a helicase. RNA 2 (about 3000 nt) encodes the 2a protein with a classic GDD RNA dependent RNA polymerase motif, and the 2b protein that is involved in suppression of host gene silencing. RNA 3 (about 2200 nt) encodes the movement protein, required for cell-to-cell and systemic movement, and the coat protein that encapsidates the RNA. The open reading frames of CMV exhibit a modular type of evolution (Roossinck, 2002). Sometimes CMV strains harbor a parasitic RNA called the satellite RNA (satRNA). The satRNAs are small (about 330-400 nt) and do not appear to encode any proteins. They are highly structured (Rodríguez-Alvarado and Roossinck, 1997), have a variety of effects on the virus and the host, and make excellent reporters for disease and evolution.
Other models we use are Cowpea chlorotic mottle virus, a relative of CMV, and an array of fungal viruses.





