title: 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.
abstract: 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.
authors.affiliation: HM.CLAUSE Seed Company, 9241 Mace Blvd, 95618, Davis, CA, USA.
authors.forename: Shaunese
authors.initials: S
authors.lastname: Lambel
authors.forename: Brenda
authors.initials: B
authors.lastname: Lanini
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Vivoda
authors.forename: Julie
authors.initials: J
authors.lastname: Fauve
authors.forename: W
authors.initials: W
authors.lastname: Patrick Wechter
authors.forename: Karen R
authors.initials: KR
authors.lastname: Harris-Shultz
authors.forename: Laura
authors.initials: L
authors.lastname: Massey
authors.forename: Amnon
authors.initials: A
authors.lastname: Levi
mesh_terms: D002874:Chromosome Mapping; D032461:Chromosomes, Plant; D029773:Citrullus / Q000235:genetics* / Q000382:microbiology; D060467:Disease Resistance / Q000235:genetics*; D005670:Fusarium; D008040:Genetic Linkage; D005838:Genotype; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology; D020641:Polymorphism, Single Nucleotide; D040641:Quantitative Trait Loci
references.citation: BMC Plant Biol. 2014 Jan 20;14:33
references.pmid: 24443961
references.citation: Theor Appl Genet. 1992 Nov;85(2-3):353-9
references.pmid: 24197326
references.citation: Genetics. 1989 Jan;121(1):185-99
references.pmid: 2563713
references.citation: Evolution. 2007 May;61(5):1017-32
references.pmid: 17492957
references.citation: PLoS One. 2011 May 04;6(5):e19379
references.pmid: 21573248
references.citation: PLoS Genet. 2013;9(12):e1003964
references.pmid: 24348260
references.citation: Plant Physiol Biochem. 2014 Jan;74:42-9
references.pmid: 24262994
references.citation: Nat Genet. 2013 Jan;45(1):51-8
references.pmid: 23179023
references.citation: Theor Appl Genet. 1987 Feb;73(4):556-62
references.pmid: 24241113
references.citation: Gene Regul Syst Bio. 2007 Sep 26;1:167-75
references.pmid: 19936086
references.citation: Nat Rev Genet. 2001 Jan;2(1):11-20
references.pmid: 11253063
references.citation: Annu Rev Phytopathol. 2006;44:135-62
references.pmid: 16602946
references.citation: BMC Plant Biol. 2008 Nov 10;8:113
references.pmid: 19000301
references.citation: Arch Biochem Biophys. 1961 May;93:369-76
references.pmid: 13697397
references.citation: Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9828-32
references.pmid: 1682921
references.citation: Plant Cell Rep. 2012 May;31(5):895-904
references.pmid: 22187088
references.citation: J Hered. 2002 Jan-Feb;93(1):77-8
references.pmid: 12011185