QTL mapping of Fusarium ear rot resistance using genotyping by target sequencing (GBTS) in maize.

Abstract

Fusarium ear rot (FER) is a global disease caused by the fungal pathogen Fusarium verticillioides. Maize FER resistance is a quantitative trait controlled by polygenes. In this study, a doubled haploid (DH) population involving 159 lines, developed from the inbred lines B73 (susceptible) and CXS161 (highly resistant), was inoculated with Fusarium verticillioides across 4-year-location environment combinations in China during 2021 and 2022. The lines were genotyped using target sequencing with a 10 K SNP array. The results showed that the estimated broad-sense heritability (H²) in each environment ranged from 0.659 to 0.871, with an overall H² of 0.805. The average genetic length between adjacent markers in the genetic map constructed using multiple single-nucleotide polymorphisms (mSNP) was smaller than that constructed using SNP, whereas the maximal genetic length was almost the same. Using a genetic map constructed with a SNP, two quantitative trait loci (QTL) were identified on chromosomes 2 and 5, which explained 7.65% and 9.58% of the phenotypic variation, respectively. Using the genetic map constructed by mSNP, four QTL were identified, explaining 6.04-12.60% of the phenotypic variation. Moreover, two kompetitive allele-specific PCR (KASP) markers were developed using single-marker analysis methods, with one KASP marker validated across a backcross population that can be effectively used to identify FER resistance. In conclusion, using mSNP for genetic map construction does not confer advantages when the population size is limited and the marker density is high. However, the mSNP-constructed map identified more minor-effect QTL despite possessing a lower likelihood of the odds (LOD) values.