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Spikelets compactness (SC) plays an important role in the yield improvement and Fusarium head blight (FHB) resistance of wheat. In this study, 151 recombinant inbred lines (RIL) derived from a cross between Yangmai 4 (YM4) and Yanzhan 1 (YZ1) and 143 RIL derived from a cross between Yangmai 5 (YM5) and YZ1 were used to construct two wheat hexaploidy genetic linkage maps, evaluate SC across three years and identify quantitative trait loci (QTL) for SC. A total of seven QTL were identified in two populations and explained the phenotypic variation ranging from 6.27% to 22.49%. Four QTL were co‐located in two genomic regions on chromosomes 2D and 6B, namely, QSc‐2D and QSc‐6B, respectively. Comparison analysis showed that QSc‐6B is a novel QTL, whereas QSc‐2D was located in the interval of Rht8. Significant additive effects of QSc‐2D and QSc‐6B on SC were observed in two RIL populations. Moreover, the positive alleles of these two QTL extremely significantly increased grain number per spike (GNS) but did not have a significantly negative effect on thousand‐grain weight (TGW), kernel length (KL) and kernel weight (KW). Whether in spray or point inoculation, QSc‐6B did not significantly influence FHB resistance in two populations. However, QSc‐2D significantly affected FHB resistance in spray inoculation in YM4/YZ1 population. A breeder‐friendly Kompetitive Allele‐Specific PCR (KASP) marker KASP_6B for QSc‐6B has been developed and verified in a set of 181 wheat cultivars/lines. Furthermore, we preliminary analysed the candidate genes within the physical interval of QSc‐6B by sequence similarity, spatial expression patterns and collinearity analysis. TraesCS6B03G1206900, TraesCS6B03G1214800 and TraesCS6B03G1218300 show specific expression in spikelet. These results provide valuable information for map‐based cloning of QSc‐6B and a useful tool for wheat breeding. [ABSTRACT FROM AUTHOR]

Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We conducted a genome-wide association study (GWAS) using the high-density wheat 90 K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016–2017 (abbr. as 2017) and 2017–2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90 K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65–14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85–622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09–547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection. [ABSTRACT FROM AUTHOR]