Abstract.
QTLs associated with products of the carotenoid pathway, including lycopene and the provitamin A carotenes α- and β-carotene, were investigated in two unrelated F2 carrot populations, derived from crosses between orange cultivated B493 and white wild QAL (Population 1), and orange cultivated Brasilia and dark-orange cultivated HCM (Population 2). The mapping populations of 160 and 180 individuals, respectively, were analyzed with single-marker and interval-mapping statistical approaches, using coupling linkage maps for each parent. Single markers were selected for further analysis based on the Wilcoxon sum-rank non-parametric test. Interval mapping performed with Population 2 detected four, eight, three, one and five putative QTLs associated with accumulation of ξ-carotene, α-carotene, β-carotene, lycopene and phytoene, respectively. Among these, the major QTLs explained 13.0%, 10.2%, 13.0%, 7.2% and 10.2% of total phenotypic variation. In Population 1 single-marker analysis identified loci explaining up to 13.8%, 6.8%, 19.3%, 5.7%, and 17.5%, respectively, of total phenotypic variation for these same carotenoids. Overall analysis demonstrated clustering of these QTLs associated with the carotenoid pathway: the AFLP loci AACCAT178-Q and AAGCAG233-Q, on linkage group 5, explained 17.8%, 22.8% and 23.5% of total phenotypic variation for ζ-carotene, phytoene and β-carotene in Population 1. Two major clusters of QTLs, with LOD scores greater than 1.8, mapped to intervals no larger than 2 cM for ζ-carotene, β-carotene, α-carotene and lycopene on linkage group 3, and for ζ-carotene and phytoene on linkage group 9, and these explained 3.7% to 13.0% of variation for each carotenoid product. Thus, these results suggest that clustering of related pathway loci is favored during evolution, since closely linked "pathway mates" are not easily separated by recombination.
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Santos, .C., Simon, .P. QTL analyses reveal clustered loci for accumulation of major provitamin A carotenes and lycopene in carrot roots. Mol Gen Genomics 268, 122–129 (2002). https://doi.org/10.1007/s00438-002-0735-9
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DOI: https://doi.org/10.1007/s00438-002-0735-9