Abstract

Tobacco mosaic virus (TMV) and Tomato mosaic virus (ToMV) cause a serious disease in tomato, with systemic mosaic symptoms and losses in fruit yield and quality. Both viruses are closely related tobamoviruses, plus stranded RNA viruses with a rod like particle structure. The genomic structure of TMV and ToMV has been well characterized, as a positivesense single-stranded RNA genome that encodes at least four proteins (Goelet et al. 1982; Ohno et al. 1984; Canto et al. 2004). The 130 kDa methyltransferase/helicase and the 180 kDa RNA dependent RNA polymerase are translated directly from the genomic RNA using the same first initiation codon, the latter is synthesised by the read-through of the amber termination codon of the 130 kDa protein gene. The movement protein (MP) and the coat protein (CP) are translated from their respective subgenomic mRNAs, which are synthesised during the replication cycle. Involvement of the 130 kDa and 180 kDa proteins in intracellular replication has been demonstrated by deletion or substitution mutants of each protein (Ishikawa et al. 1986). It has also been shown that the MP is involved in cellto-cell transport (Meshi et al. 1987), and that the CP is involved in long-distance movement (Saito et al. 1990; Hilf and Dawson, 1993). In tomato, TMV infection is more or less a rare event because the virus is soon competed out in tomato populations by ToMV, which is more adapted to this host plant.

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