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Powdery mildew (PM), caused by the biotrophic fungus Podosphaera xanthii, drastically reduces the yield and quality of melon (Cucumis melo L.). Knowledge on the genetic control and high throughput molecular markers linked with resistance against this disease are essential for breeding programs. The bioassay study of the F1 and F2 populations derived from the parents, ‘PMR 5’ (♂) and ‘SCNU1154’ (♀) revealed a monogenic dominant nature of resistance to the devastating race, race 5. Besides, we developed three SNP based high resolution melting markers, PMm-HRM-1, PMm-HRM-2, and PMm-HRM-3 based on the previously identified SNPs on chromosome 12 and validated those using 10 melon lines and 137 F2 population. Among these, the SNP of marker PMm-HRM-1 causes a missense mutation (Lysine → Glutamic acid) in the LRR region of MELO3C002393 and were able to distinguish the resistant vs susceptible genotypes from 10 diverse melon population and the segregating F2 population with more than 90% genotyping efficiency. Other two markers were based on intergenic SNPs and had more than 80% genotyping efficiency F2 population. These markers will be helpful to melon breeders to develop melon cultivars resistant to P. xanthii race 5 via marker assisted breeding programs.

Background Bacterial fruit blotch (BFB), a disease caused by Acidovorax citrulli, results in significant economic losses in melon. The causal QTLs and genes for resistance to this disease have yet to be identified. Resistance (R)-genes play vital roles in resistance to plant diseases. Since the complete genome sequence of melon is available and genome-wide identification of R-genes has been performed for this important crop, comprehensive expression profiling may lead to the identification of putative candidate genes that function in the response to BFB. Results We identified melon accessions that are resistant and susceptible to BFB through repeated bioassays and characterized all 70 R-genes in melon, including their gene structures, chromosomal locations, domain organizations, motif distributions, and syntenic relationships. Several disease resistance-related domains were identified, including NBS, TIR, LRR, CC, RLK, and DUF domains, and the genes were categorized based on the domains of their encoded proteins. In addition, we profiled the expression patterns of the genes in melon accessions with contrasting levels of BFB resistance at 12 h, 1 d, 3 d, and 6 d after inoculation with A. citrulli. Six R-genes exhibited consistent expression patterns (MELO3C023441, MELO3C016529, MELO3C022157, MELO3C022146, MELO3C025518, and MELO3C004303), with higher expression levels in the resistant vs. susceptible accession. Conclusion We identified six putative candidate R-genes against BFB in melon. Upon functional validation, these genes could be targeted for manipulation via breeding and biotechnological approaches to improve BFB resistance in melon in the future.