Fusarium wilt, caused by Fusarium oxysporum f. sp. melonis (F.o.m), is a worldwide soilborne disease of melon (Cucumis melo L.). The most eVective control measure available is the use of resistant varieties. Resistance to races 0 and 2 of this fungal pathogen is conditioned by the dominant gene Fom-1. An F 2 population derived from the 'Charentais-Fom1' £ 'TRG-1551' cross was used in combination with bulked segregant analysis utilizing the random ampliWed polymorphic DNA (RAPD) markers, in order to develop molecular markers linked to the locus Fom-1. Four hundred decamer primers were screened to identify three RAPD markers (B17 649 , V01 578 , and V06 1092 ) linked to Fom-1 locus. Fragments ampliWed by primers B17 649 and V01 578 were linked in coupling phase to Fom1, at 3.5 and 4 cM respectively, whereas V06 1092 marker was linked in repulsion to the same dominant resistant allele at 15.1 cM from the Fom-1 locus. These RAPDs were cloned and sequenced in order to design primers that would amplify only the target fragment. The derived sequence characterized ampliWed region (SCAR) markers SB17 645 and SV01 574 (645 and 574 bp, respectively) were present only in the resistant parent. The SV06 1092 marker ampliWed a band of 1092 bp only in the susceptible parent. These markers are more universal than the CAPS markers developed by Brotman et al. (Theor Appl Genet 10:337-345, 2005). The analysis of 24 melon accessions, representing several melon types, with these markers revealed that diVerent melon types behaved diVerently with the developed markers supporting the theory of multiple, independent origins of resistance to races 0 and 2 of F.o.m.

Melon Fusarium wilt (MFW), caused by Fusarium oxysporum f. sp. melonis (Fom), is one of the most destructive diseases of melon (Cucumis melo L.). The development and deployment of resistant cultivars is generally considered to be the best approach to control MFW. Based on the host resistance genes associated with variants of this pathogen, Fom isolates were classified into four physiological races designated 0, 1, 2, and 1,2. Two dominant resistance genes, Fom-1 and Fom-2, control resistance to races 0 and 2, and 0 and 1, respectively. Fom isolates classified as race 1,2 are able to induce disease in melon lines carrying the above resistance genes. Many sources of resistance to Fom races 0, 1, and 2 have been reported. Partial resistance to race 1,2 controlled by polygenic recessive genes was only detected in a few Far Eastern melon accessions, except for the breeding line BIZ where complete resistance was described. Identification of DNA markers tightly linked to genes conferring resistance to Fom has immediate application in MFW resistance breeding programs. The Fom-2 gene has been cloned, and it encodes a protein with a nucleotide binding site (NBS) and leucine-rich repeats domain (LRR). Based on the sequence of this domain, some molecular markers linked to this gene were developed. Several DNA markers linked to Fom-1 have also been described. However, the usefulness of these markers was variety-dependent. Therefore, their combined use would be very useful in marker assisted selection for introducing resistance to Fom races 0 and 2 in melon. Recently, these markers were used for the positional cloning of this gene, which encoded a protein with a NBS–LRR domains that shows similarity to the toll and interleukin-1 receptores (TIR). Regarding Fom race 1,2, nine QTL were detected on five linkage groups by composite interval mapping. In this paper we review the current knowledge of MFW disease, and focus on genetic resistance to Fom and marker-assisted selection for resistance.

Fusarium wilt incited by Fusarium oxysporum f. sp. melonis (

The inheritance of the resistance to Fusarium oxysporum f. sp. melonis (F.o.m.) races 0 and 2 in