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The locus RTM1 is necessary for restriction of long-distance movement of tobacco etch virus in Arabidopsis thaliana without causing a hypersensitive response or inducing systemic acquired resistance. The RTM1 gene was isolated by map-based cloning. The deduced gene product is similar to the ␣-chain of the Artocarpus integrifolia lectin, jacalin, and to several proteins that contain multiple repeats of a jacalin-like sequence. These proteins comprise a family with members containing modular organizations of one or more jacalin repeat units and are implicated in defense against viruses, fungi, and insects.resistance

SummaryScreens of Arabidopsis thaliana for susceptibility to tobacco etch virus (TEV) revealed that each of 10 ecotypes were able to support genome replication and cell-to-cell movement in inoculated leaves. However, only four ecotypes, including C24 and La-er, supported complete infections in which TEV was able to replicate and move from cell to cell and long distances through the vasculature. The rates of cell-to-cell movement of a reporter-tagged TEV strain (TEV-GUS) in inoculated leaves of C24 and Columbia (Col-3) were similar, and infection foci continued to expand in both ecotypes through 10 days post-inoculation. No visible or microscopic hypersensitive or cell death responses were evident in inoculated leaves of Col-3 plants. Infection of neither C24 nor Col-3 plants with TEV-GUS resulted in induction of PR-1a gene expression, which is normally associated with active defence responses and systemic acquired resistance. The genetic basis for the restriction of longdistance movement of TEV-GUS in Columbia was investigated using C24 ⍥ Col-3 crosses and backcrosses and using La-er ⍥ Col-0 recombinant inbred lines. A dominant locus conditioning the restricted TEV infection phenotype was identified on chromosome 1 between markers ATEAT1 and NCC1 at approximately 14 cM in both genetic analyses. This locus was designated RTM1 (restricted TEV movement 1). It is proposed that RTM1 mediates a restriction of long-distance movement through a mechanism that differs substantially from those conditioned by the dominant resistance genes normally associated with genefor-gene interactions.

The idea that viruses move through plants in two distinct modes was accurately concluded by G. Samuel in a 1934 paper describing the transport of tobacco mosaic virus (TMV) through solanaceous hosts: "lt is considered that these facts favour the theory of a slow cell to cell movement of the virus via the plasmodesmen, combined with a rapid distribution through the plant via the phloem" (Samuel, 1934). It is now firmly established that plant viruses move from cell to cell and over long distances by exploiting and modifying preexisting pathways for macromolecular movement within cells, between cells, and between organs. In this review, we focus on the roles of vira1 and host components in the movement of viruses through these pathways. Exhaustive coverage of all aspects of movement is not possible, but the reader is referred to several excellent reviews that emphasize various facets of short-and long-range virus transport (

The roles of the capsid protein (CP) and the CP coding sequence of tobacco etch potyvirus (TEV) in genome amplification were analyzed. A series of frameshift-stop codon mutations that interrupted translation of the CP coding sequence at various positions were introduced into the TEV genome. A series of 3 deletion mutants that lacked the CP coding sequence beyond each of the frameshift-stop codon mutations were also produced. In addition, a series of 5 CP deletion mutants were generated. Amplification of genomes containing either frameshiftstop codon insertions after codons 1, 59, 103, and 138 or genomes containing the corresponding 3 deletions of the CP coding sequence was reduced by 100-to 1,000-fold relative to that of the parental genome in inoculated protoplasts. In contrast, a mutant containing a frameshift-stop codon after CP position 189 was amplified to 27% of the level of the parental virus, but the corresponding 3 deletion mutant lacking codons 190 to 261 was nonviable. Deletion mutants lacking CP codons 2 to 100, 2 to 150, 2 to 189, and 2 to 210 were amplified relatively efficiently in protoplasts, but a deletion mutant lacking codons 2 to 230 was nonviable. None of the amplification-defective frameshift-stop codon or deletion mutants was rescued in transgenic cells expressing TEV CP, although the transgenic CP was able to rescue intercellular movement defects of replicationcompetent CP mutants. Coupled with previous results, these data led to the conclusions that (i) TEV genome amplification requires translation to a position between CP codons 138 and 189 but does not require the CP product and (ii) the TEV CP coding sequence contains a cis-active RNA element between codons 211 and 246. The implications of these findings on mechanisms of RNA replication and genome evolution are discussed.