Begomoviruses are plant DNA viruses for which recombination plays a key role in driving evolution. However, little is known about how frequently begomovirus recombinants arise in mixed infected plants. To tackle this issue, co-infections of tomato with monopartite begomoviruses associated with the tomato yellow leaf curl disease, Tomato yellow leaf curl Sardinia virus and Tomato yellow leaf curl virus, have been studied as a model system. The frequency of recombinant genotypes in the progeny populations was evaluated at several times post inoculation. Recombinants constituted a significant proportion of the viral population. Interestingly, not all regions of the genome contributed equally to genetic exchange. In addition to the intergenic region, a known hot spot for recombination, a second hot spot region was found. Implication of secondary structure sequence features in cross-over sites is suggested, which might favor discontinuous DNA replication with the replication complex switching between homologous regions of DNA templates.
Tomato yellow leaf curl disease (TYLCD) is a severe threat to tomato crops worldwide and is caused by Tomato yellow leaf curl virus (TYLCV) and several other begomoviruses (genus Begomovirus, family Geminiviridae). Host plant resistance is the best TYLCD control method but limited sources of resistance are available. In this study, two Solanum habrochaites TYLCD-resistance sources, EELM-388 and EELM-889, were found after a wide germplasm screening and were further characterized. A consistent resistance to the widely distributed strain TYLCV-IL was observed when plants were inoculated by Bemisia tabaci or by agroinoculation using an infectious clone, with no symptoms or virus accumulation observed in inoculated plants. Moreover, the resistance was effective under field conditions with high TYLCD pressure. Two independent loci, one dominant and one recessive, were associated with EELM-889 resistance. The study shows these loci to be distinct from that of the resistance gene (Ty-1 gene) commonly deployed in commercial tomato cultivars. Therefore, both kinds of resistance could be combined to provide improved resistance to TYLCD. Four additional TYLCD-associated viruses were challenged, showing that the resistance always prevented symptom expression, although systemic infection could occur in some cases. By using chimeric and mutant expression constructs, the C4 protein was shown to be associated with the ability to result in effective systemic infection.
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