Mapping and validation of Fusarium wilt race 2 resistance QTL from Citrullus amarus line USVL246-FR2.

KEY MESSAGE: Fon race 2 resistant QTLs were identified on chromosomes 8 and 9. Families homozygous for resistance alleles at a haplotype of three KASP markers had 42% lower disease severity than those with susceptible alleles in an independent, interspecific validation population confirming their utility for introgression of Fusarium wilt resistance. Fusarium oxysporum f. sp. niveum (Fon) race 2 causes Fusarium wilt in watermelon and threatens watermelon production worldwide. Chemical management options are not effective, and no resistant edible watermelon cultivars have been released. Implementation of marker-assisted selection to develop resistant cultivars requires identifying sources of resistance and the underlying quantitative trait loci (QTL), developing molecular markers associated with the QTL, and validating marker-phenotype associations with an independent population. An intraspecific Citrullus amarus recombinant inbred line population from a cross of resistant USVL246-FR2 and susceptible USVL114 was used for mapping Fon race 2 resistance QTL. KASP markers were developed (N = 51) for the major QTL on chromosome 9 and minor QTL on chromosomes 1, 6, and 8. An interspecific F2:3 population was developed from resistance donor USVL246-FR2 (C. amarus) and a susceptible cultivar 'Sugar Baby' (Citrullus lanatus) to validate the utility of the markers for introgression of resistance from the wild crop relative into cultivated watermelon. Only 16 KASP markers segregated in the interspecific C. amarus/lanatus validation population. Four markers showed significant differences in the separation of genotypes based on family-mean disease severity, but together explained only 16% of the phenotypic variance. Genotypes that inherited homozygous resistant parental alleles at three KASP markers had 42% lower family-mean disease severity than homozygous susceptible genotypes. Thus, haplotype analysis was more effective at predicting the mean disease severity of families than single markers. The haplotype identified in this study will be valuable for developing Fon race 2 resistant watermelon cultivars.

Genome-Wide Association Mapping and Genomic Prediction of Fusarium Wilt Race 2 Resistance in the USDA Citrullus amarus Collection.

Fusarium wilt caused by Fusarium oxysporum f. sp. niveum (Fon) race 2 is a serious disease in watermelon and can reduce yields by 80%. Genome-wide association studies (GWAS) are a valuable tool in dissecting the genetic basis of traits. Citrullus amarus accessions (n = 120) from the USDA germplasm collection were genotyped with whole-genome resequencing, resulting in 2,126,759 single nucleotide polymorphic (SNP) markers that were utilized for GWAS. Three models were used for GWAS with the R package GAPIT. Mixed linear model (MLM) analysis did not identify any significant marker associations. FarmCPU identified four quantitative trait nucleotides (QTN) on three different chromosomes (i.e., chromosomes 1, 5, and 9), and Bayesian-information and linkage-disequilibrium iteratively nested keyway (BLINK) identified one QTN on chromosome 10 as significantly associated with Fon race 2 resistance. FarmCPU identified four QTN that explained 60% of Fon race 2 resistance, and the single QTN from BLINK explained 27%. Relevant candidate genes were found within the linkage disequilibrium (LD) blocks of these significant SNPs, including genes encoding aquaporins, expansins, 2S albumins, and glutathione S-transferases which have been shown to be involved in imparting resistance to Fusarium spp. Genomic predictions (GP) for Fon race 2 resistance using all 2,126,759 SNPs resulted in a mean prediction accuracy of 0.08 with five-fold cross-validation employing genomic best linear unbiased prediction (gBLUP) or ridge-regression best linear unbiased prediction (rrBLUP). Mean prediction accuracy with gBLUP leave-one-out cross-validation was 0.48. Thus, along with identifying genomic regions associated with Fon race 2 resistance among the accessions, this study observed prediction accuracies that were strongly influenced by population size.

The use of PI 277012-derived Fusarium head blight resistance QTL in winter wheat breeding.

Fusarium head blight (FHB) caused by Fusarium graminearum results in substantial grain yield and quality losses in common wheat (Triticum aestivum L.). Genetic resistance is partial but crucial for effective, integrated management of the disease. Host resistance is conditioned by numerous small effect quantitative trait loci (QTL) that are strongly affected by the environment and genetic background. Qfhb.rwg-5A.1 and Qfhb.rwg-5A.2 (PI 277012 is the source for both genes) are two recently discovered FHB resistance QTL that also occur in spring wheat GP80 (PI 277012 derivative). To transfer the PI 277012 resistance from GP80 to hard winter wheat (HWW), GP80 was first crossed with Novus-4. The F1 hybrid was crossed with SY Monument, following which marker-selected progeny were crossed with, and backcrossed to, ND Noreen. To potential carriers of FHB resistance QTL among the 22 F1 of the ND Noreen cross, simple sequence repeat (SSR) markers, Illumina 90 K single nucleotide polymorphism (SNP) haplotypes and greenhouse FHB Type II resistance tests were done. Likely homozygotes for Qfhb.rwg.5A.1 and Qfhb.rwg.5A.2, were selected and backcrossed to ND Noreen. In the B1F1, 131 plants were evaluated for SNP haplotypes, SSR markers and FHB resistance. Nine B1F2:3 lines were derived, and their resistance confirmed in a third greenhouse FHB trial. The results suggested that eight lines had higher resistance and were comparable to GP80 with the Qfhb.rwg-5A.2 markers occurring in all eight and the Qfhb.rwg-5A.1 markers occurring in four lines. The eight selections constitute a valuable HWW resistance breeding resource.