Fusarium wilt, caused by Fusarium oxysporum f. sp. melonis (FOM), is a main disease of melon (Cucumis melo L.). FOM 1.2 is the most widespread and detrimental variant of FOM, causing substantial economic losses under severe disease conditions. Current information suggests that resistance to race 1.2 (FOM 1.2) is controlled by multiple recessive genes and is strongly influenced by the environment. Therefore, identifying genetic polymorphisms within diverse melon populations is essential to elucidate the loci and putative candidate genes associated with resistance. The objective of this investigation was to identify single-nucleotide polymorphism (SNP) and structural variant (SV) markers associated with FOM 1.2 resistance utilizing a panel of 160 genotypes through a genome-wide association study (GWAS). Phenotypic evaluation was performed two weeks after sowing, at the first-true-leaf stage, on 2400 individual plants inoculated by the root dip method with a concentration of about 106 spores/mL. Biochemical and disease-related traits, including area under disease progress curve (AUDPC), disease severity index (DSI), standardized AUDPC (SAUDPC), latent period (LP), catalase, peroxidase activity, and ascorbate peroxidase activity were measured 35 days after inoculation. PCA identified eighty-three individual melon plants with a broad range of disease-response variation. Genotyping-by-sequencing (GBS) was conducted on these plants, resulting in the identification of 737,435 SNPs and 75,133 SVs. Evaluation of the population structure outlined four genetic groups, including one associated with germplasm highly resistant to FOM 1.2. We used SNP data to describe linkage disequilibrium (LD), which was estimated to decay at 14 kb, on average. A GWAS was performed using the Bayesian information and linkage-disequilibrium iteratively nested keyway (BLINK) method, which revealed nine SNPs significantly associated with several disease indices, namely ascorbate peroxidase activity, AUDPC, catalase, peroxidase activity, rAUDPC, and SAUDPC. Also, eight SVs were associated with AUDPC and relative area under disease progress curve (rAUDPC), including translocation and deletion types. In addition, GWAS using the fixed and random model circulating probability unification (FarmCPU) method unveiled thirteen SVs associated with rAUDPC, peroxidase activity and ascorbate peroxidase activity, including translocation and inversion types. According to the performed models of GWAS, several significant SNPs and SVs, associated with putative candidate genes, including multidrug resistance-associated protein 6 (MRP6), LOB domain-containing protein 15 (LBD15), phosphomannomutase, and NADH-ubiquinone oxidoreductase B8 subunit, which may be involved in FOM 1.2 resistance. However, these findings represent a preliminary genome-wide survey and require further validation using high-coverage or long-read sequencing approaches. The results provide remarkable insights into the genetic control of FOM 1.2 resistance and valuable information for the implementation of the putative molecular markers identified in this study in melon breeding programs.
Bozorgmehr et al. (Sun,) studied this question.