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  • Author or Editor: Marisol Luís-Arteaga x
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Melon necrotic spot virus (MNSV) has been found affecting melon (Cucumis melo L.) crops. At present the only known resistance in melon is controlled by a single recessive gene, nsv. The presence of nsv in a melon genotype has been correlated with the lack of necrotic lesions on the mechanically inoculated cotyledons. Thus, in a screening program for MNSV resistance, melon genotypes that developed necrotic lesions in the inoculated cotyledons were discarded. However, in this paper we show that some melon accessions mechanically inoculated with MNSV do develop local necrotic lesions, therefore showing the absence of the gene nsv, but fail to develop the systemic symptoms typical of diseased plants under the screening conditions. In some of these accessions the influence of the temperature on the development of systemic symptoms was studied. The results showed that, depending on the accession, temperatures under 25 or 20 °C enhanced the systemic development of the disease. One of the tested varieties, `Doublon', did not develop systemic symptom at any of the tested temperatures (15, 17.5, 20, 22.5, 25, 27.5, and 30 °C). In this variety, the lack of systemic symptoms was correlated to the lack of virus infection of these tissues based upon ELISA results. MNSV was not detected in the uninoculated parts of the plant, and seems to remain confined to the local lesions produced on the cotyledons following the mechanical inoculation. Restriction of viral multiplication and/or cell-to-cell movement could explain the pattern of viral distribution in this variety. This reaction was observed in the `Doublon' plants mechanically inoculated with each of five isolates of MNSV tested, including an isolate that overcomes the nsv gene resistance.

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The recessive allele (nsv) of the NSV gene confers resistance to the Carmovirus melon necrotic spot virus (MNSV) in melon (Cucumis melo L.). Using an F2 population obtained from the cross between the resistant Korean accession PI 161375 and a susceptible line of `Piel de Sapo', we have mapped the NSV locus to linkage group 11 (G11) of the melon genome. Additional markers closely linked to NSV were developed by bulked segregant analysis (BSA) using a doubled haploid progeny population derived from the same cross. A detailed map of the NSV region was constructed containing 10 markers spanning a distance of 17.7 cM. The nearest flanking markers to NSV were two amplified fragment length polymorphisms (AFLPs) (CTA/ACG-115 and CTA/ACG-120) and one random amplified polymorphic DNA (RAPD) (OPD08-0.80) separated by 5.9 cM. Two more markers, ACC/ACC-110 and OPX15-1.06, cosegregated with NSV.

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