Fusarium wilt, caused by the soilborne fungus Fusarium oxysporum f.sp.niveum(FON), is one of the most economically important diseases of watermelon (Citrullus lanatus) worldwide. FON has been divided into three races (races 0, 1, and 2) determined by differential pathogenicity assays. Most commercial cultivars are resistant to races 0 and 1; whereas none are resistant to race 2. Few morphological and isozyme variations are seen in the cultivated watermelon, but molecular markers, such as random amplified polymorphic DNA (RAPD), amplified fragment length polymorphisms (AFLPs) and simple sequence repeats (SSRs), have been shown to generate several polymorphisms. Segregating populations, derived from a cross between watermelon cultivar New Hampshire Midget, susceptible to all three races of FON and the resistant C. lanatus plant introduction PI 296341, were used to detect molecular markers linked to Fusarium wilt resistance. In a preliminary experiment, more than 180 10-mer primers were screened against the parents and the F1. Informative RAPD primers were identified and used in conjunction with AFLP and SSR markers to generate a genome map.
QTL mapping for Fusarium wilt resistance based on the whole-genome resequencing and their association with functional genes in Raphanus sativus