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.