Fusarium ear rot (FER), caused by Fusarium verticillioides, is a devastating disease that substantially reduces maize yield and compromises kernel quality. To investigate the genetic and molecular basis of resistance, an F2 population derived from a cross between the resistant inbred line 3IBZ2 and the susceptible inbred line KW5G321 was analysed. By integrating bulked segregant analysis sequencing (BSA-Seq) with RNA sequencing (RNA-Seq), a major quantitative trait locus (QTL), designated qFER4, was identified on chromosome 4. Genetic analysis further demonstrated that qFER4 confers resistance through partial dominance. Transcriptome profiling of the resistant line revealed 7684 and 7906 differentially expressed genes (DEGs) at 36 and 72 h post inoculation (hpi), respectively. These DEGs were significantly enriched in defence-related biological processes and pathways, including phenylpropanoid biosynthesis, jasmonic acid signalling, MAPK cascades, and plant-pathogen interactions. By combining QTL mapping with transcriptome analyses, four candidate genes within the qFER4 interval were screened. Sequence analysis identified extensive structural variations in the promoter and coding regions of Zm00001d053393, including a premature stop codon predicted to lead to a gain-of-function mutation. In contrast, the other three genes exhibited only minor promoter polymorphisms with identical coding sequences between the parental lines. Overall, this study identifies a novel major-effect QTL and candidate gene associated with FER resistance, providing a foundation for gene function and a valuable genetic resource for breeding FER-resistant maize varieties.
Sun et al. (Mon,) studied this question.