Research Video: Roossinck Lab

Ph.D., Microbiology and Immunology, 1986, University of Colorado
Joined the Noble Foundation in 1991

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?

Cucumber mosaic virus

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.