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Fusarium verticillioides  can be transmitted via seeds and cause systemic infection in maize ( Zea mays  L.); its mycotoxin has harmful effects on animal and human health. We combined QTL mapping in recombinant inbred line (RIL) populations with a genome-wide association study (GWAS) of 217 diverse maize lines using 224,152 single nucleotide polymorphisms (SNPs) under controlled conditions to determine the genetic architecture of  F. verticillioides  seed rot (FSR) resistance. Our study identified 8 quantitative trait loci (QTLs) and 43 genes associated with 57 SNPs that were correlated with FSR resistance through linkage mapping and GWAS, respectively. Among these, there were three candidate genes, namely  GRMZM2G0081223, AC213654.3_FG004 , and  GRMZM2G099255 , which were detected in both linkage mapping and GWAS. Furthermore, the near-isogenic lines (NILs) containing  GRMZM2G0081223 , which also had a susceptible parent background, were found to have a significantly improved level of resistance. In addition, the expression profile of the three candidate genes revealed that they all respond to the infection following inoculation with  F. verticillioides . These genetic analyses indicate that FSR resistance is controlled by loci with minor effect, and the polymerization breeding of lines with beneficial alleles and candidate genes could improve FSR resistance in maize.

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Dissecting the genetic architecture of Fusarium verticillioides seed rot resistance in maize by combining QTL mapping and genome-wide association analysis