A Genetic Locus Associated with Resistance to Fusarium oxysporum f. sp. niveum Race 2 in Citrullus lanatus-type Watermelon

Abstract

Fusarium wilt of watermelon (Citrullus lanatus), caused by Fusarium oxysporum f. sp. niveum (FON), is a devastating soil-borne disease limiting watermelon production across the world. Although many watermelon cultivars have been bred for resistance to FON races 0 and 1, the only released cultivars that are resistant to FON 2 are nonharvested pollenizers. The lack of FON 2–resistant edible cultivars is thought to be associated with linkage drag and/or preferential inheritance patterns observed when crossing the resistant, wild source (Citrullus amarus), with edible watermelon. A potential way to overcome these obstacles is to use a resistant C. lanatus as the source of resistance and to develop molecular markers to increase the efficiency of selection. Here we describe the identification of a quantitative trait locus (QTL) associated with FON 2 resistance in watermelon. The genotyping by sequencing (GBS) platform was used to generate single nucleotide polymorphisms (SNPs) in an F2 population (n = 178) developed from a cross between UGA147 (resistant) and ‘Charleston Gray’ (susceptible). Five hundred and one SNPs were placed on the watermelon physical map and used in the mapping of QTL. F3 lines were phenotyped for resistance to FON 2 in the greenhouse. An intermediate QTL associated with resistance to FON 2 was identified on chromosome 11 (Qfon11). This QTL is a potential target for marker-assisted selection (MAS) for FON 2 resistance in watermelon.