A hybrid plant RNA virus made by transferring the noncapsid movement protein from a rod-shaped to an icosahedral virus is competent for systemic infection.

For many plant RNA viruses, multiple viral gene products, including noncapsid movement proteins and capsid proteins, contribute to the spread of infection within plants. The extent to which these factors interact to support infection spread is not known, but, for movement protein mutants of certain viruses, the inability of coinoculated "helper" viruses to complement defective movement has suggested a possible requirement for coadaptation between noncapsid movement proteins and other virus factors. To test directly for required coadaptation, the 3a movement protein gene of cowpea chlorotic mottle virus, an icosahedral bromovirus, was replaced with the nonhomologous 30-kDa movement protein gene of sunn-hemp mosaic virus, a rod-shaped, cowpea-adapted tobamovirus. The resulting hybrid virus is competent for systemic infection of cowpea, with systemic infection dependent upon expression of the 30-kDa gene. In view of the dramatic differences between cowpea chlorotic mottle virus and sunn-hemp mosaic virus in genetic organization and particle morphology, the ability of the hybrid to systemically infect cowpea implies that the tobamovirus 30-kDa movement protein functions independently of sequence-specific interactions with other viral components or sequences. Similarly, the required contribution of bromovirus capsid protein to infection movement appears to be independent of specific interaction with the natural 3a movement protein. In addition to other implications concerning movement protein and coat protein function, the results are consistent with the possibility that two or more distinguishable transfer processes may be involved in crossing different tissue barriers to achieve full systemic spread of infection.