ARS | Publication request: QUANTITATIVE TRAIT LOCI AND METABOLIC PATHWAYS: GENETIC CONTROL OF THE CONCENTRATION OF MAYSIN, A CORN EARWORM RESISTANCE FACTOR, IN MAIZE SILKS.

Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 1996
Publication Date: N/A

Interpretive Summary: Resistance to the corn earworm (CEW), a major silk- and kernel-feeding insect pest of maize in the United States, is due largely to the concentration of a chemical in the silks known as maysin. Our study sought to determine the genes controlling maysin concentration in a population developed from a cross between high-maysin and low-maysin inbred lines. By comparing maysin concentrations in silks of individual plants with their DNA patterns, we found that a single region of chromosome 1 accounted for 58% of the variation in maysin content and a second region, on chromosome 9 explained 11% of the variation. Both regions contain previously reported genes that are hypothesized to affect the synthesis of maysin or related chemicals. Results of this study will assist maize breeders wishing to select for increased levels of CEW resistance.

Technical Abstract: Antibiosis toward the corn earworm (CEW), Helicoverpa zea (Boddie), in maize, Zea mays L., silks is due primarily to the concentration of maysin and related flavone glycosides. Our study sought to determine the genetic factors controlling maysin concentration in the population (GT114 x GT119)F2, derived from a cross of a high- by a low-maysin parent. Silk maysin concentrations and RFLP genotypes at loci encoding flavonoid pathway enzymes or linked loci were determined for 285 F2 plants. Single-factor analysis of variance indicated that 58.0% of the phenotype variance in maysin concentration was accounted for by the p1 region on chromosome 1, which showed additive gene action. The p1 locus is a transcription activator for portions of the flavonoid pathway. A region on chromosome 9, represented by the marker umc105 and near the reported location of the brown pericarp 1 (bp1) locus, accounted for 10.8% of the variance, with the allele from the low-maysin parent contributing to higher maysin values. Gene action of this region was dominant for low maysin, but was only expressed in the presence of a functional p1 allele. The model explaining the greatest proportion of phenotypic variance (75.9%) included p1, umc105, umc166b (a locus on chromosome 1 that is not, to our knowledge, closely linked to reported flavonoid pathway loci), r1, and two epistatic interaction terms, p1 x umc105 and p1 x r1. Our results provide evidence for the importance of regulatory loci and for the complex interplay among different branches of the flavonoid pathway in the expression of this trait.