Last database update for these data: 2006-12-20 - Data extracted on 2009-04-14 from the database.
| No | Title | Period | Description | Projects | Crops | Viruses | Host plants |
|---|---|---|---|---|---|---|---|
| 1 | Use of wild accessions and near isogenic lines of Lycopersicon hirsutum for the identification of host factors involved in the susceptibility to Cucumber mosaic virus and its satellite RNA. | 2002 and after | Several accessions of wild and cultivated species of the genus Lycopersicon, including L. esculentum (tomato), L. hirsutum, L. chilense, L. pimpinellifolium, L. pennellii and L. peruvianum, were tested for their susceptibility to combinations of Cucumber mosaic virus (CMV) with variants of satellite RNA (satRNA) co-inducing diverse disease phenotypes in tomato. The following CMV preparations have been used for the characterisation of Lycopersicon spp./CMV/satRNA interactions: a) CMV-Fny (no satRNA); b) CMV-FB (Fny + a Benign satRNA variant, symptomless on tomato); c) CMV-FS (Fny + a tomato Stunting-inducing satRNA variant); d) CMV-FN (Fny + a tomato Necrosis-inducing satRNA). CMV-Fny induced on all hosts the typical leaf malformation (shoestring, reduced leaflet blade), and no resistance was observed on any of the tested genotypes. CMV-FB induced on all hosts a phenotype characterised by latent infection accompanied by the down-regulation of viral RNA replication, referred to as LIDR (Latent Infection, Down-Regulation). Interestingly, LIDR was observed also on some wild Lycopersicon accessions inoculated with CMV-FS and CMV-FN that are aggressive on tomato. In particular, accessions of L. chilense showed LIDR with both the aggressive CMV/satRNA combinations tested, whereas accessions of L. hirsutum and L. pennellii showed LIDR upon inoculation with CMV-FS, but susceptibility to systemic necrosis induced by CMV-FN. A screening of 99 near isogenic lines, containing single introgressions from L. hirsutum accession LA1777 in the L. esculentum cv. E6206 genetic background (Monforte and Tanksley, Genome/Génome 43: 803, 2000), was undertaken to map host factors determining differential susceptibility to CMV/satRNA in Lycopersicon spp. Observing a temporary resistance to CMV-FS on one of these lines, a possible host factor interfering with stunting, but not with systemic necrosis, was mapped genetically to L. hirsutum chromosome 6. Other loci were identified, correlating with changes in symptoms expression rather than with absence of symptoms. From these preliminary studies the following conclusions are drawn: a) CMV/satRNAs diverse symptoms (leaf malformation, stunting, necrosis) on host Lycopersicon spp. are due to alterations of apparently individual and uncoupled pathways; b) L. chilense can be a source of gene(s) responsible for protection from CMV/satRNA-induced lethal necrosis; c) the LIDR phenotype appears to be regulated by a multigenic character not directly transferable to cultivated tomato genotypes. | 1. Molecular and genetic bases involved in the susceptibility of Lycopersicon spp. to cucumber mosaic virus and its satellite RNA | Tomato | Cucumber mosaic virus | Lycopersicon esculentum |
| 2 | Characterization Of Synergy Between Cucumber Mosaic Virus And Potato Virus Y In Tomato. | 2002 and after | We investigated on some biological and molecular characteristics of the synergistic effects shown by Cucumber mosaic virus (CMV) and Potato virus Y (PVY) on tomato. Plants inoculated with CMV-Fny exhibited the typical leaf reduction symptoms. We generated two pseudorecombinant strains with different pathogenetic properties inoculating CMV-Fny RNA1 and RNA3 in addition to, respectively, CMV-LS RNA2 (CMV-FLF) and the CMV-Fny RNA2 mutant 209m3D2b (CMV-D2b). CMV-FLF, like the RNA2 donor strain CMV-LS, induced very mild symptoms on tomato, whereas CMV-D2b, a modified CMV-Fny that cannot translate the 2b protein, did not infect tomato systemically. Tomato plants infected with PVY-SON41 showed symptomless infection. CMV-D2b spread systemically when inoculated on PVY-infected tomato plants, revealing that the loss of movement functions of the 2b protein mutant was complemented by PVY analogue functions, as shown also by electron microscopy and immunogold labeling. With the exception of PVY + CMV-D2b, which induced a mild phenotype, symptoms resulted exacerbated in mixed infections, confirming a role for the 2b protein as an enhancer of symptom severity. Symptom severity in mixed infections correlated with increased viral spread and RNA accumulation levels more evident at 60 days post-infection, both in the case of CMV and PVY, although especially the latter virus showed heterogeneity in the distribution throughout the plant and sample-to-sample variation. Small interfering RNA (siRNA) accumulation, the typical hallmark of RNA silencing in virus-infected plants, varied in different PVY/CMV combinations showing positive correlation with the corresponding viral RNA levels, and suggested no role of CMV and PVY RNA silencing suppressors, 2b and HC-Pro proteins respectively, in preventing RNA silencing directed against both viruses in natural infections. | 1. CMV- and PVY-mediated RNA silencing in mixed infections in tomato | Tomato | Cucumber mosaic virus Potato virus Y |
Lycopersicon esculentum |