|Holland, Jim - Jim|
Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/17/2006
Publication Date: 6/20/2006
Citation: Robertson, L., Jines, M., Balint Kurti, P.J., Kleinschmidt, C., White, D., Payne, G., Maragos, C.M., Holland, J.B. 2006. Qtl mapping for fusarium ear rot and fumonisin contamination resistance in two populations of maize (zea mays). Crop Science 46:1734-1743. Interpretive Summary: Ear rots of corn (maize) caused by Fusarium fungi both lower yield and contaminate grain with fumonisins, a family of mycotoxins that adversely affects animal and human health. The objective of this work was to identify genetic resistance to both ear rot and fumonisin contamination in maize and to ask whether some genes provided resistance to both. Genes for resistance for both rot and fumonisin contamination were identified in two different families of maize plants and several genes were indeed shown to affect both traits. This information will be very useful to breeders trying to improve resistance to this important disease.
Technical Abstract: Fusarium verticillioides (Sacc.) Nirenberg (synonym F. moniliforme Sheldon) (teleomorph: Gibberella moniliformis) and F. proliferatum (Matsushima) Nirenberg (teleomorph: G. intermedia) are fungal pathogens of maize (Zea mays L.) that cause ear rot and contaminate grain with fumonisins, a family of mycotoxins that adversely affects animal and human health. The objective of this study was to identify QTL for resistance to Fusarium ear rot and fumonisin contamination in two maize populations, comprised of 215 BC1F1:2 families from the first backcross of GE440 to FR1064 (GEFR) and 143 recombinant inbred lines from the cross NC300 × B104 (NCB). QTL mapping was used to investigate whether QTL were consistent across populations and the genetic relationships between resistances to ear rot and to fumonisin contamination. In the GEFR population, six QTL explained 43.6% of the phenotypic variation for mean ear rot resistance across environments and nine QTL with one epistatic interaction explained 66.6% of the variation for mean fumonisin concentration across environments. In the NCB population, five QTL explained 31.3% of the phenotypic variation for mean ear rot resistance across environments and six QTL and three epistatic interactions explained 50.1% of the phenotypic variation for mean fumonisin concentration across environments. Three QTL in the GEFR population and four QTL in the NCB population affected both ear rot and fumonisin concentration. Three ear rot and three fumonisin contamination resistance QTL mapped to similar positions in the two populations. One QTL localized to chromosome four appeared to be consistent for both traits across both populations.