Tobamoviruses, mostly isolated from solanaceous plants, may represent ancient virus lineages that have codiverged with their hosts. Recently completed nucleotide sequences of six nonsolanaceous tobamoviruses allowed assessment of the codivergence hypothesis and support a third subgroup within tobamoviruses. The genomic sequences of 12 tobamoviruses and the partial sequences of 11 others have been analyzed. Comparisons of the predicted protein sequences revealed three clusters of tobamoviruses, corresponding to those infecting solanaceous species (subgroup 1), those infecting cucurbits and legumes (subgroup 2), and those infecting crucifers. The orchid-infecting odontoglossum ringspot tobamovirus was associated with subgroup 1 genomes by its coat and movement protein sequences, but with the crucifer-pathogenic tobamoviruses by the remainder of its genome, suggesting that it is the progeny of a recombinant. For four of five genomic regions, subgroup 1 and 3 genomes were equidistant from a subgroup 2 genome chosen for comparison, suggesting uniform rates of evolution. A phylogenetic tree of plant families based on the tobamoviruses they harbor was congruent with that based on rubisco sequences but had a different root, suggesting that codivergence was tempered by rare events of viruses of one family colonizing another family. The proposed subgroup 3 viruses probably have an origin of virion assembly in the movement protein gene, a large (25-codon) overlap of movement and coat protein open reading frames, and a comparably shorter genome. Codon-position-dependent base compositions and codon prevalences suggested that the coat protein frame of the overlap region was ancestral. Bootstrapped parsimony analysis of the nucleotides in the overlap region and of the sequences translated from the -1 frame (the subgroup 3 movement protein frame) of this region produced trees inconsistent with those deduced from other regions. The results are consistent with a model in which a no or short overlap organization was ancestral. Despite encoding of subgroup 2 and 3 movement protein C-termini by nonhomologous nucleotides, weak similarities between their amino acid sequences suggested convergent sequence evolution.
Despite a potentially key role in cell-to-cell communication, plant intercellular connections-the plasmodesmata-have long been a biological "black box." Little is known about their protein composition, regulatory mechanisms, or transport pathways. However, recent studies have shed some light on plasmodesmal function. These connections have been shown to actively traffic proteins and protein-nucleic acid complexes between plant cells. This review describes these transport processes-specifically, cell-to-cell movement of plant viruses as well as endogenous cellular proteins-and discusses their possible mechanism(s). For comparison and to provide a broader perspective on the plasmodesmal transport process, the current model for nuclear import, the only other known example of transport of large proteins and protein-nucleic acid complexes through a membrane pore, is summarized. Finally, the function of plasmodesmata as communication boundaries within plant tissue is discussed.
SummaryHeavy metals, such as cadmium, have a significant impact on plant physiology. However, their potential effect on plant-pathogen interaction, an important biological process, has not been examined. This study shows that exposure of tobacco plants to non-toxic concentrations of cadmium completely blocked viral disease caused by turnip vein clearing virus. Cadmium-mediated viral protection was due to inhibition of the systemic movement of the virus, i.e. its spread from the inoculated into uninoculated leaves. Exposure of plants to cadmium had no effect on viral replication, assembly and local movement within the inoculated leaf. Analysis of the viral presence in different tissues suggested that cadmium treatment inhibited virus exit from the vascular tissue into uninoculated leaves rather than its entry into the host plant vasculature. Higher, toxic levels of cadmium did not produce this inhibitory effect on viral movement, allowing the systemic spread of the virus and development of the viral disease. These observations suggest that cadmium-induced viral protection requires a relatively healthy, unpoisoned plant in which non-toxic levels of cadmium may trigger the production of cellular factors which interfere with the viral systemic movement.
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