Professor Rick Nelson

Richard S. Nelson, Ph.D

Professor

Noble Researcher since 1988

rsnelson@noble.org

Nelson Lab

Ph.D., Biology, 1985, University of Illinois

Research emphasis: Molecular and cellular biology of virus movement in plants

The overall objective of research within the Nelson laboratory is to understand how plant RNA viruses move and accumulate in their hosts. Specifically, we are studying the route by which viruses move from initially infected cells into cells within the vascular tissue for transport to other parts of the plant. We are also interested in the route viruses use to escape from the vascular tissue to initiate an infection in the upper uninoculated leaves and virus replication in this tissue. This research necessarily includes the study of gene silencing and silencing suppression in this tissue.

In order to identify the viral proteins or nucleic acid sequences necessary for viral passage from cell-to-cell and leaf-to-leaf and its subsequent accumulation we have assembled a battery of site-directed or truncated cDNA mutants of tobacco mosaic virus strains from which infectious transcripts can be produced. These mutants have differing movement and systemic accumulation phenotypes allowing us to identify the viral sequences necessary for these activities. Dr. X.S. Ding has initiated an independent project to study the cell-to-cell and leaf-to-leaf movement and subsequent accumulation of viruses infecting monocot plants.

It is apparent that virus movement and systemic accumulation requires the presence of various viral proteins interacting with specific host factors, and we are attempting to characterize these host factors. In addition, we are identifying the cell boundaries that limit infection.

We utilize molecular biological, immunocytochemical, in situ localization, microinjection and classical and confocal fluorescence microscopy technique to answer the questions we pose.

By identifying viral and host factors important for virus movement and accumulation, the function of these nucleic acids and proteins, and the location of their effect, we can begin to design rational strategies to make plants resistant to vascularly-derived viral infection. Such a novel resistance strategy could be combined with other proven strategies for obtaining transgenic plants resistant to viral challenge, thereby creating a potentially impenetrable barrier to viral infection and spread due to multiple mechanisms of protection. In addition, we are utilizing our knowledge in this area to study the function of host genes in monocotyledonous and dicotyledonous plants through virus-induced gene silencing.

See Also:
2005 Scientific Report: Nelson Laboratory