SNP Discovery and QTL Mapping of Sclerotinia Basal Stalk Rot Resistance in Sunflower using Genotyping‐by‐Sequencing

Abstract

Basal stalk rot (BSR), caused by the ascomycete fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a serious disease of sunflower (Helianthus annuus L.) in the cool and humid production areas of the world. Quantitative trait loci (QTL) for BSR resistance were identified in a sunflower recombinant inbred line (RIL) population derived from the cross HA 441 ´ RHA 439. A genotyping-bysequencing (GBS) approach was adapted to discover single nucleotide polymorphism (SNP) markers. A genetic linkage map was developed comprised of 1053 SNP markers on 17 linkage groups (LGs) spanning 1401.36 cM. The RILs were tested in five environments (locations and years) for resistance to BSR. Quantitative trait loci were identified in each environment separately and also with integrated data across environments. A total of six QTL were identified in all five environments: one of each on LGs 4, 9, 10, 11, 16, and 17. The most significant QTL, Qbsr-10.1 and Qbsr-17.1, were identified at multiple environments on LGs 10 and 17, explaining 31.6 and 20.2% of the observed phenotypic variance, respectively. The remaining four QTL, .1, were detected in only one environment on LGs 4, 9, 11, and 16, respectively. Each of these QTL explains between 6.4 and 10.5% of the observed phenotypic variation in the RIL population. Alleles conferring increased resistance were contributed by both parents. The potential of the Qbsr-10.1 and Qbsr-17.1 in marker-assisted selection (MAS) breeding are discussed. Sclerotinia sclerotiorum (Lib.) de Bary is a necrotrophic fungus with a vast host range of >400 broadleaf species (Boland and Hall, 1994). The fungus causes three distinctly different diseases on sunflower: BSR or wilt, midstalk rot (MSR), and head rot. This fungal pathogen is characterized by its ability to produce long-term survival structures called sclerotia, which individually consist of masses of hyphae surrounded by a hard, black, protective rind. Depending on environmental conditions, sclerotia can germinate myceliogenically, and cause root infection, or carpogenically, producing apothecia then ascospores and infect aboveground parts of host plants (Gulya et al., 1997;Bolton et al., 2006). Unlike other hosts, BSR symptoms start from a root infection resulting from myceliogenic germination of sclerotia. Midstalk rot commonly begins as a leaf infection, while head rot infection begins on capitula. Both MSR and head rot symptoms are incited by airborne ascospores Univ., Fargo, ND 58102, USA. Mention of trade names or commercial products in this article is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the USDA. The USDA is an equal opportunity provider and employer.

Genotyping-by-Sequencing Uncovers the Introgression Alien Segments Associated with Sclerotinia Basal Stalk Rot Resistance from Wild Species—I. Helianthus argophyllus and H. petiolaris

“…Notably, seven of the eight resistant introgression lines developed in this study had the alien segments detected in LG8, suggesting that new QTL of BSR resistance from the wild species are also present in this linkage group. The two QTL on LG10 detected by Amouzadeh et al (2013) and Talukder et al (2016) are located at a region between 253.4 and 281. 3 Mb, while ~34 polymorphic SNPs (66.7% of the shared SNPs) in LG10 that detected alien segments in three introgression lines were also located in this region (Table 8).…”

“…Currently, there are no cultivated sunflower inbred lines or commercial hybrids that possess an acceptable level of resistance to Sclerotinia (Hahn, 2002; Gulya, 2005; Talukder et al, 2014, 2016). In an effort to manage sunflower Sclerotinia disease, numerous wild Helianthus species were screened for their reaction to Sclerotinia head rot and stalk rot.…”

“…The five QTL for the percentage of necrotic area, based on controlled growth chamber tests, were located on LGs 1, 3, 8, 10, and 17 with the small effects, and each QTL explained between 0.5 and 3.2% of the observed phenotypic variance in the RIL population. Talukder et al (2016) identified two major BSR resistance QTL on LGs 10 and 17 in multiple environments of a RIL population derived from a cross of HA 441/RHA 439, each explaining 31.6 and 20.2% of the observed phenotypic variance, respectively. An additional four QTL were also detected on LGs 4, 9, 11, and 16 in only one environment.…”

“…However, quantitative genetic variations among some varieties have been described (Tourvieille et al, 1996; Degener et al, 1998, 1999; Gulya et al, 2010; Talukder et al, 2014). Previous efforts to characterize BSR resistance indicated that the trait is quantitatively inherited for which the majority of the genetic variation is due to additive gene effects (Mestries et al, 1998; Van Becelaere and Miller, 2004; Talukder et al, 2016). Thus, breeding sunflower for Sclerotinia BSR resistance has relied on the introgression of genetic factors from various partially resistant accessions using recurrent selection or pedigree breeding methods (Miller and Gulya, 1999, 2006).…”

Registration of Oilseed Sunflower Germplasm HA‐BSR1 Highly Tolerant to Sclerotinia Basal Stalk Rot

“…Breeding using resistant germplasm is the most economic and efficient disease management strategy used by most sunflower breeding programs. However, BSR resistance breeding is relatively complex, as resistance is controlled by multiple genes, each with a small effect (Davar et al, 2010; Talukder et al, 2014b), some of which have been mapped to the sunflower genome and linked with DNA markers (Davar et al, 2010; Amouzadeh et al, 2013; Talukder et al, 2016). Although no sunflower hybrids are completely resistant to BSR, significant variation in tolerance to this disease has been reported in currently available germplasm resources (Talukder et al, 2014a).…”