Current Researchers: R. N. Beachy
Previous Researchers: M. Bendahmane, J. Fitchen, G. Lettieri, Yao, M. Koo, S. Asurmendi

For more than 75 years, agriculturists have known that inoculating crop plants with a mild strain of a virus can prevent infection by a severe strain. The mechanism that accounted for this protective effect was unknown, but researchers reasoned that incorporation of viral genes into plants may be able to produce the same effect.

In the mid-1980s, Dr. Roger Beachy and his co-workers conducted pioneering experiments in which they inserted into tobacco plants the gene that codes for the coat protein (CP) of the tobacco mosaic virus (TMV). They found that the transgenic plants carrying the CP gene did not show symptoms of infection after exposure to TMV; the plants were effectively virus resistant. This type of resistance is referred to as coat protein-mediated resistance (CP-MR). Researchers working in Dr. Beachy's laboratory have continued the work of deciphering the mechanism responsible for virus resistance with the goal of enhancing the effectiveness of CP-MR.

Studies of the mechanisms of coat protein-mediated resistance:

• The presence of TMV CP reduces the disassembly of infecting virus particles:

  When TMV particles are introduced into a plant cell, the outer layer consisting of coat protein molecules, begins to disassemble. This exposes the viral RNA genome which can then serves as mRNA for the viral replicase, the enzyme responsible for replicating the viral genome. In a plant cell that contains CP produced by the transgene, virus disassembly is inhibited and fewer viral particles are replicated. The greater the amount of CP, the higher the degree of resistance. Furthermore, CP-MR is more effective against tobamoviruses that are closely related to TMV than against distantly related tobamoviruses. Work continues on finding how CP prevents disassembly.

   

• Analyses of selected CP mutants are providing information about the mechanisms of CP-mediated resistance.

  Certain CP mutants confer higher levels of CP-mediated resistance than does wild type CP. Mutations in CP that cause increased interactions between CP molecules led to greater resistance.

  Like wild type CP, certain mutants reduce the number of sites of infection in transgenic plants, while other mutants had little effect on infection, but limited replication and/or disease.

  Ongoing studies include structural analyses of selected CP mutants to clarify the interactions within and between CP molecules that are responsible for increasing the levels of CP-MR.