Genetics of Melon yellows virus resistance derived from Cucumis melo ssp agrestis

The Melon yellows virus (MYV), a whitefly-transmitted closterovirus, is one of the major pathogens causing crop losses in protected melons in southeas tern Spain. An accession of the wild Asiatic Cucumis melo ssp. agrestis (Cm a) shows resistance to MYV infection. Results indicate the participation of two resistance mechanisms in this source: firstly, an antixenotic reaction against Trialeurodes vaporariorum, the disease vector, and secondly, resis tance to the virus. The combined effect of these two mechanisms confers Cma a higher level of resistance, expressed as a delayed and milder infection. The genetics of resistance to the Melon yellows closterovirus have been stu died in two families derived from Cma. As under natural infection condition s, the effect of antixenosis and virus resistance cannot be distinguished, a biometrical model that permits separation of the two resistance mechanism s operating in the same resistant source, has been proposed to determine ge netic control of MYV resistance. The genetic analysis has been conducted by fitting the disease progress cur ves of each generation to the biometrical model instead of fitting the fina l disease ratios. The scoring of disease incidence over time allows for the comparison of data from assays conducted in different conditions (2 years/ 4 transplanting dates), thus reinforcing the analysis. The results agree with a simple control of the resistance to MYV derived fr om Cma, with incomplete penetrance of the gene and partial dominance of res istance. The effect of antixenosis on the spread of this plant virus is hig hly significant in Cma, but not in segregant generations. Since there do not exist crossability barriers between this accession and t he cultivated melon, Cma could be readily used in breeding programmes to ob tain melon varieties resistant to MYV.