ArticleMolecular plant pathology2015
Four sequence positions of the movement protein of Cucumber mosaic virus determine the virulence against cmv1-mediated resistance in melon.
Article in Molecular plant pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Introgression line libraries in melon (Molecular breeding : new strategies in plant improvement · 2026Review
- Article
- Comprehensive proteomic profiling of Cucumber mosaic virus infection: identifying key proteins and pathways involved in resistance and susceptibility in melon.BMC plant biology · 2025Article
- Possibility of genome editing for melon breeding.Breeding science · 2024Article
- Article
- Mutations in CmVPS41 controlling resistance to cucumber mosaic virus display specific subcellular localization.Plant physiology · 2023Article
- Determinants of Virus Variation, Evolution, and Host Adaptation.Pathogens (Basel, Switzerland) · 2022Review
- Review
- Article
- A mutation in the melon Vacuolar Protein Sorting 41prevents systemic infection of Cucumber mosaic virus.Scientific reports · 2017Article
- cmv1 is a gate for Cucumber mosaic virus transport from bundle sheath cells to phloem in melon.Molecular plant pathology · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The resistance to a set of strains of Cucumber mosaic virus (CMV) in the melon accession PI 161375, cultivar 'Songwhan Charmi', is dependent on one recessive gene, cmv1, which confers total resistance, whereas a second set of strains is able to overcome it. We tested 11 strains of CMV subgroups I and II in the melon line SC12-1-99, which carries the gene cmv1, and showed that this gene confers resistance to strains of subgroup II only and that restriction is not related to either viral replication or cell-to-cell movement. This is the first time that a resistant trait has been correlated with CMV subgroups. Using infectious clones of the CMV strains LS (subgroup II) and FNY (subgroup I), we generated rearrangements and viral chimaeras between both strains and established that the determinant of virulence against the gene cmv1 resides in the first 209 amino acids of the movement protein, as this region from FNY is sufficient to confer virulence to the LS clone in the line SC12-1-99. A comparison of the sequences of the strains of both subgroups in this region shows that there are five main positions shared by all strains of subgroup II, which are different from those of subgroup I. Site-directed mutagenesis of the CMV-LS clone to substitute these residues for those of CMV-FNY revealed that a combination of four of these changes [the group 64-68 (SNNLL to HGRIA), and the point mutations R81C, G171T and A195I] was required for a complete gain of function of the LS MP in the resistant melon plant.
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