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Abstract

In tomato, infections by tomato mosaic virus are controlled by durable Tm-2(2) resistance. In order to gain insight into the processes underlying disease resistance and its durability, we cloned and analysed the Tm-2(2) resistance gene and the susceptible allele, tm-2. The Tm-2(20 gene was isolated by transposon tagging using a screen in which plants with a destroyed Tm-2(2) gene survive. The Tm-2(2) locus consists of a single gene that encodes an 861 amino acid polypeptide, which belongs to the CC-NBS-LRR class of resistance proteins. The putative tm-2 allele was cloned from susceptible tomato lines via PCR with primers based on the Tm-2(2) sequence. Interestingly, the tm-2 gene has an open reading frame that is comparable to the Tm-2(2) allele. Between the tm-2 and the Tm-2(2) polypeptide 38 amino acid differences are present of which 26 are located in the second half of the LRR-domain. Susceptible tomato plants, which were transformed with the Tm-2(2) gene, displayed resistance against ToMV infection. In addition, virus specificity, displayed by the Tm-2(2) resistance was conserved in these transgenic lines. To explain the durability of this resistance, it is proposed that the Tm-2(2)-encoded resistance is aimed at the Achilles' heel of the virus.

Molecular Markers for Tm-2 Alleles of Tomato Mosaic Virus Resistance in Tomato

“…AF536199 is the accession in GenBank that contains the sequence of the tm-2 susceptible allele; AF536200 is the sequence Tm-2 resistance allele; and AF536201 is the sequence of Tm-2 2 resistance allele. The size of the AF536199 sequence of the allele tm-2 is 2820 bp; AF536200 is 2819 bp; and AF536201 is 9837 bp [3]. Primers Tm2RS-f2, Tm2RS-r2, Tm2RS-f3, and Tm2RS-r3 were designed for the three sequences of AF536199, AF536200, and AF536201; Tm2S-f1, Tm2S-r1, Tm2S-f2, and Tm2S-r2 for AF536199 only; Tm2R-f1c and Tm2R-r4 for both AF536200 and AF536201; Tm2R-r3 for AF536200 only; and Tm2aR-r3 for AF536201 only (Table 2).…”

“…The practical and effective method of controlling this disease is through introducing major resistance gene(s). So far, three genes, Tm-1, Tm-2 and Tm-2 2 of ToMV resistance have been reported and used in tomato cultivar development [1][2][3][4][5]. The Tm-1 gene was introgressed into S. lycopersicum from the wild tomato species S. habrochaites and mapped to chromosome 5 and it conferred resistance to ToMV strains 0 and 2 [1,4,6,7].…”

“…The Tm-1 gene has been cloned and the sequences were stored in GenBank with five accessions DJ344478 to DJ344481, and DJ344505. The other two genes Tm-2 and Tm-2 2 were introgressed from S. peruvianum and were located closely to the centromere of chromosome 9 and are considered to be allelic and Tm-2 conferred resistance to ToMV strains 0 and 1, whereas allele Tm-2 2 conferred resistance to ToMV strains 0, 1 and 2 [2,3,5,[8][9][10]. Molecular markers have been widely used in genetic mapping and marker-assisted selection (MAS) for disease resistance in tomato [6].…”

Genetic resistance for the sustainable control of plant virus diseases: breeding, mechanisms and durability

“…However, most extensively studied examples of dominant resistance correspond to genes encoding CC-NBS-LRR proteins that control resistance responses. Some of these examples include Tm-2 2 , which confers extreme resistance to ToMV in tomato and tobacco (Weber et al 1993;Lanfermeijer et al 2003Lanfermeijer et al , 2004, and Rx, which confers extreme resistance to most Potato virus X (PVX) strains in potato (Bendahmane et al 1997(Bendahmane et al , 1999. Analysis carried out in resistant protoplasts showed that Rx-mediated resistance is elicited by the PVX coat protein and is effective against unrelated viruses such as CMV Bendahmane et al 1995).…”

“…Mutations responsible for gains of virulence also frequently induce fitness costs to the virus in plants devoid of the corresponding resistance. This was shown in several instances (Agudelo-Romero et al 2008;Lanfermeijer et al 2003;Jenner et al 2002;Desbiez et al 2003;Ayme et al 2006) although other examples suggest that virulent strains can be at least as fit as avirulent ones (Chain et al 2007;Sorho et al 2005). However, in these latter examples, it was not determined whether mutations outside the virulence factor also contributed to fitness variations.…”