Tomato mosaic virus (ToMV) causes a serious loss of yield and fruit quality in tomato crops. To control ToMV, three resistance genes, Tm-1 , Tm-2 , and Tm-2 2 from wild tomato species were introduced into commercial tomato cultivars. Soon after, however, single and, rarely, double-resistance-breaking virus strains for Tm-1 and Tm-2 emerged. Sequence analysis of a Tm-1 / Tm-2 double-resistance-breaking virus, designated ToMV1-2, revealed 30 nucleotide substitutions compared with wild-type ToMV. Of these, six substitutions result in amino acid exchanges. Two exchanges are in the methyl transferase/helicase domain of the ToMV1-2 130/180-kDa proteins (D-1097 to V, R-1100 to Q), two exchanges are found in the 30-kDa movement protein (MP; E-52 to K, E-133 to K), and two exchanges are in the coat protein (I-22 to V, A-87 to S). Construction of chimeric full-length viral cDNA clones containing the base substitutions resulting in altered amino acids, either in the 130/180 kDa proteins or the MP, revealed that the amino acid exchanges in the 130/180-kDa proteins enable ToMV1-2 to break the Tm-1 resistance, while those in the MP enable ToMV1-2 to overcome the Tm-2 resistance. Furthermore, a novel Tm-1 / Tm-2 double-resistance-breaking virus was generated by combining the Tm-1 -breaking domain of ToMV1-2 and the MP of a new virus, ToMV2, containing the amino acid exchanges E-133 to K and N-135 to S. Together, the data suggest that double-resistance-breaking ToMV1-2 may have resulted from recombination between Tm-1 and Tm-2 single resistance-breaking virus strains.
Archives of Virology – Springer Journals
Published: May 1, 2007
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