Abstract

The Tm-2(2) resistance gene is used in most commercial tomato cultivars for protection against infection with tomato mosaic virus (ToMV). It has been suggested that Tm-2(2) resistance interferes with viral cell-to-cell movement in plants; ToMV strain ToMV-2(2) requires two amino acid (aa) exchanges in the carboxy-terminal region of the viral 30-kDa movement protein (at positions 238 and 244) to overcome Tm-2(2) resistance. For further analysis of this region of the 30-kDa protein, two stop codons were introduced into ToMV movement proteins at aa positions 235 and 237, leading to deletion of the terminal 30 aa. The mutant virus strains were able to infect wild-type tomato plants systemically, suggesting the carboxy-terminal portion of the ToMV 30-kDa protein is dispensable for virus transport in tomato. Even more important, the deletion mutants overcame the Tm-2(2) resistance gene. These data indicate the carboxy-terminal domain of the ToMV movement protein serves as a recognition target in the context of the Tm-2(2) resistance gene. Furthermore, expression of the 30-kDa movement protein from wild-type ToMV, but not from ToMV-2(2), in transgenic tomato plants with the Tm-2(2) resistance gene led to elicitation of a necrotic reaction in tomato seedlings, showing that the 30-kDa protein on its own is able to induce the plant's defense reaction.

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