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The involvement of plasmodesmata (PD) in viral systemic infection has long been accepted. An extensive body of supporting literature has been provided by electron microscopic analysis of infected leaves and stems (26). These studies almost always showed viral particles lodged within structurally mod ified PD that were located between infected cells. Images of this type led to the concept that plant viruses must have evolved a mechanism(s) that enables them to move, from cell to cell, by physically modifying PD to allow the passage of the encapsidated form of each virus (i.e. diameter of icosahedral virus particles range from 18-80 nm, whereas filamentous or flexuous rod shaped particles have diameters ranging from 10-25 nm). Although the ultra structural approach to the study of viral infection provided essential infor mation on the cytopathological effects of viruses and their cellular distribution, within the plant, it did not provide information on the actual mechanism(s) involved in viral movement. With the advent of molecular biology, this limi tation has now been removed. Over the past decade great progress has been made in identifying and characterizing the viral genes and their products that enable plant viruses to move from cell to cell and long distances within the plant. Rapid advances in plant molecular virology, in concert with recent advances
Lucas et al. (Thu,) studied this question.