Strain-specific and recessive QTLs involved in the control of partial resistance to Fusarium oxysporum f. sp. melonis race 1.2 in a recombinant inbred line population of melon

• Published in: Theoretical and applied genetics 2005-06, Vol.111 (1), p.65-74
• Main Authors: Perchepied, L, Dogimont, C, Pitrat, M
• Format: Article
• Language: English
• Subjects: alleles; Biological and medical sciences; Chromosome Mapping; Classical genetics, quantitative genetics, hybrids; Crosses, Genetic; Cucumis melo; Cucumis melo - genetics; disease resistance; DNA Primers; dominance (genetics); epistasis; Epistasis, Genetic; Fundamental and applied biological sciences. Psychology; Fusarium; Fusarium oxysporum; Fusarium oxysporum f. sp. melonis; Fusarium wilt; genetic markers; Genetics; Genetics of eukaryotes. Biological and molecular evolution; Genomics; Immunity, Innate - genetics; inbred lines; Life Sciences; Melonis; melons; Nucleic Acid Amplification Techniques; partial resistance; pathotypes; Phenotype; phenotypic variation; Plant Diseases - genetics; Plant Diseases - microbiology; Polymorphism, Restriction Fragment Length; Pteridophyta, spermatophyta; Quantitative Trait Loci; races; recessive genes; recombinant inbred lines; Vegetals
• ISSN: 0040-5752; 1432-2242
• DOI: 10.1007/s00122-005-1991-y

Fusarium oxysporum f. sp. melonis (FOM) causes serious economic losses in melon (Cucumis melo L.). Two dominant resistance genes have been identified, Fom-1 and Fom-2, which provide resistance to races 0 and 2 and races 0 and 1, respectively, however FOM race 1.2 overcomes these resistance genes. A partial resistance to FOM race 1.2 that has been found in some Far East accessions is under polygenic control. A genetic map of melon was constructed to tag FOM race 1.2 resistance with DNA markers on a recombinant inbred line population derived from a cross between resistant (Isabelle) and susceptible (cv. Vedrantais) lines. Artificial root inoculations on plantlets of this population using two strains, one that causes wilting (FOM 1.2w) and one that causes yellowing (FOM 1.2y), resulted in phenotypic and genotypic data that enabled the identification of nine quantitative trait loci (QTLs). These QTLs were detected on five linkage groups by composite interval mapping and explained between 41.9% and 66.4% of the total variation. Four digenic epistatic interactions involving seven loci were detected and increased the total phenotypic variation that was explained. Co-localizations between QTLs and resistance gene homologs or resistance genes, such as Fom-2 and Vat, were observed. A strain-specific QTL was detected, and some QTLs appeared to be recessive.