QTL mapping of resistance to Pseudoperonospora cubensis clade 1, mating type A2, in Cucumis melo.

KEY MESSAGE: This is the first identification of QTLs underlying resistance to Pseudoperonospora cubensis in Cucumis melo using a genetically characterized isolate. Pseudoperonospora cubensis, causal organism of cucurbit downy mildew (CDM), is one of the largest threats to cucurbit production in the eastern USA. Currently, no Cucumis melo (melon) cultivars have significant levels of resistance. Additionally, little is understood about the genetic basis of resistance in C. melo. Recombinant inbred lines (RILs; N = 169) generated from a cross between the resistant melon breeding line MR-1 and susceptible cultivar Ananas Yok'neam were phenotyped for CDM resistance in both greenhouse and growth chamber studies. A high-density genetic linkage map with 5,663 binned SNPs created from the RIL population was utilized for QTL mapping. Nine QTLs, including two major QTLs, were associated with CDM resistance. Of the major QTLs, qPcub-10.1 was stable across growth chamber and greenhouse tests, whereas qPcub-8.2 was detected only in growth chamber tests. qPcub-10.1 co-located with an MLO-like protein coding gene, which has been shown to confer resistance to powdery mildew and Phytophthora in other plants. This is the first screening of C. melo germplasm with a genetically characterized P. cubensis isolate.

QTL mapping of resistance to Fusarium oxysporum f. sp. niveum race 2 and Papaya ringspot virus in Citrullus amarus.

KEY MESSAGE: A Citrullus amarus mapping population segregating for resistance to Fusarium oxysporum f. sp. niveum race 2 and Papaya ringspot virus was used to identify novel QTL, important for the improvement in watermelon disease resistance. Multiple disease screens of the USDA Citrullus spp. germplasm collection have highlighted the value of Citrullus amarus (citron melon or wild watermelon) as a resource for enhancing modern watermelon cultivars (Citrullus lanatus) with resistance to a broad range of fungal, bacterial and viral diseases of watermelon. We have generated a genetic population of C. amarus segregating for resistance to two important watermelon diseases: Fusarium wilt (caused by the fungus Fusarium oxysporum f. sp. niveum; Fon race 2) and Papaya ringspot virus-watermelon strain (PRSV-W). QTL mapping of Fon race 2 resistance identified seven significant QTLs, with the major QTL representing a novel genetic source of resistance and an opportunity for gene pyramiding. A single QTL was associated with resistance to PRSV-W, which adhered to expectations of a prior study indicating a single-gene recessive inheritance in watermelon. The resistance loci identified here provide valuable genetic resources for introgression into cultivated watermelon for the improvement in disease resistance.

A GBS-SNP-based linkage map and quantitative trait loci (QTL) associated with resistance to Fusarium oxysporum f. sp. niveum race 2 identified in Citrullus lanatus var. citroides.

KEY MESSAGE: A major QTL for resistance to Fusarium oxysporum f. sp. niveum race 2 was mapped to a narrow 1.2 Mb interval using a high-density GBS-SNP linkage map, the first map of Citrullus lanatus var. citroides. Fusarium wilt, a fungal disease caused by Fusarium oxysporum f. sp. niveum (Fon), devastates watermelon crop production worldwide. Several races, which are differentiated by host range, of the pathogen exist. Resistance to Fon race 2, a particularly virulent strain prevalent in the United States, does not exist in edible cultivars of the sweet cultivated watermelon Citrullus lanatus var. lanatus (Cll) and has been well described in a few plant introductions of the wild subspecies of watermelon, C. lanatus var. citroides (Clc). Clc provides a vital source of genetic diversity, as well as resistance to numerous diseases. Unfortunately, both genetic diversity and disease resistance are lacking in Cll due to the narrow genetic base. Despite the importance of Clc to continued watermelon improvement, intra-variety genetic studies are lacking. Here, we present the first Clc genetic linkage map, generated with 2495 single nucleotide polymorphisms developed through genotyping-by-sequencing, and use it to identify quantitative trait loci associated with Fon race 2 resistance. Multiple QTL mapping in a Clc F2:3 population (N = 173) identified one major and four minor QTL. The major QTL explained 43% of the variation in Fon race 2 resistance and was delimited to a 1.2-Mb interval on chromosome 9, a region spanning 44 genes.

A major QTL associated with Fusarium oxysporum race 1 resistance identified in genetic populations derived from closely related watermelon lines using selective genotyping and genotyping-by-sequencing for SNP discovery.

KEY MESSAGE: A major quantitative trait locus (QTL) for Fusarium oxysporum Fr. f. sp. niveum race 1 resistance was identified by employing a "selective genotyping" approach together with genotyping-by-sequencing technology to identify QTLs and single nucleotide polymorphisms associated with the resistance among closely related watermelon genotypes. Fusarium wilt is a major disease of watermelon caused by the soil-borne fungus Fusarium oxysporum Schlechtend.:Fr. f. sp. niveum (E.F. Sm.) W.C. Snyder & H.N. Hans (Fon). In this study, a genetic population of 168 F3 families (24 plants in each family) exhibited continuous distribution for Fon race 1 response. Using a "selective genotyping" approach, DNA was isolated from 91 F2 plants whose F3 progeny exhibited the highest resistance (30 F2 plants) versus highest susceptibility (32 F2 plants), or moderate resistance to Fon race 1 (29 F2 plants). Genotyping-by-sequencing (GBS) technology was used on these 91 selected F2 samples to produce 266 single nucleotide polymorphism (SNP) markers, representing the 11 chromosomes of watermelon. A major quantitative trait locus (QTL) associated with resistance to Fon race 1 was identified with a peak logarithm of odds (LOD) of 33.31 and 1-LOD confidence interval from 2.3 to 8.4 cM on chromosome 1 of the watermelon genetic map. This QTL was designated "Fo-1.1" and is positioned in a genomic region where several putative pathogenesis-related or putative disease-resistant gene sequences were identified. Additional independent, but minor QTLs were identified on chromosome 1 (LOD 4.16), chromosome 3 (LOD 4.36), chromosome 4 (LOD 4.52), chromosome 9 (LOD 6.8), and chromosome 10 (LOD 5.03 and 4.26). Following the identification of a major QTL for resistance using the "selective genotyping" approach, all 168 plants of the F 2 population were genotyped using the SNP nearest the peak LOD, confirming the association of this SNP marker with Fon race 1 resistance. The results in this study should be useful for further elucidating the mechanism of resistance to Fusarium wilt and in the development of molecular markers for use in breeding programs of watermelon.