Abstract
BackgroundFusarium ear rot (FER) caused by Fusarium verticillioides is a major disease of maize that reduces grain yield and quality globally. However, there have been few reports of major loci for FER were verified and cloned.ResultTo gain a comprehensive understanding of the genetic basis of natural variation in FER resistance, a recombinant inbred lines (RIL) population and one panel of inbred lines were used to map quantitative trait loci (QTL) for resistance. As a result, a total of 10 QTL were identified by linkage mapping under four environments, which were located on six chromosomes and explained 1.0–7.1% of the phenotypic variation. Epistatic mapping detected four pairs of QTL that showed significant epistasis effects, explaining 2.1–3.0% of the phenotypic variation. Additionally, 18 single nucleotide polymorphisms (SNPs) were identified across the whole genome by genome-wide association study (GWAS) under five environments. Compared linkage and association mapping revealed five common intervals located on chromosomes 3, 4, and 5 associated with FER resistance, four of which were verified in different near-isogenic lines (NILs) populations. GWAS identified three candidate genes in these consistent intervals, which belonged to the Glutaredoxin protein family, actin-depolymerizing factors (ADFs), and AMP-binding proteins. In addition, two verified FER QTL regions were found consistent with Fusarium cob rot (FCR) and Fusarium seed rot (FSR).ConclusionsThese results revealed that multi pathways were involved in FER resistance, which was a complex trait that was controlled by multiple genes with minor effects, and provided important QTL and genes, which could be used in molecular breeding for resistance.
Highlights
Fusarium ear rot (FER) caused by Fusarium verticillioides is a major disease of maize that reduces grain yield and quality globally
These results revealed that multi pathways were involved in FER resistance, which was a complex trait that was controlled by multiple genes with minor effects, and provided important quantitative trait loci (QTL) and genes, which could be used in molecular breeding for resistance
Among these QTL, three QTL were located on chromosome 4 and the one WQ6 between markers mmc0371 and A007339 had the largest resistance effect for Fusarium ear rot, which could explain more than 9.3% of the phenotypic variation
Summary
Fusarium ear rot (FER) caused by Fusarium verticillioides is a major disease of maize that reduces grain yield and quality globally. FER reduces the yield and quality of harvested maize and is fatal to humans and animals, which consume the contaminated grain containing mycotoxins from some of the Fusarium spp. In a RIL population from NC300 × B104, Robertson et al [17] found the genomic and phenotypic correlations between FER and fumonisin accumulation is 0.87 and 0.64, respectively, indicating that it was possible to select lines with reduced FER and fumonisin contamination at the same time [17] These strategies require us to understand the genetics of resistance clearly, and identify the alleles that can significantly reduce the hazard from F. verticillioides [16]
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