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Association mapping of morphological traits in wild and captive zebra finches: reliable within,but not between populations
Authors:Ulrich Knief  Holger Schielzeth  Niclas Backström  Georg Hemmrich‐Stanisak  Michael Wittig  Andre Franke  Simon C Griffith  Hans Ellegren  Bart Kempenaers  Wolfgang Forstmeier
Institution:1. Department of Behavioural Ecology and Evolutionary Genetics, Max Planck Institute for Ornithology, Seewiesen, Germany;2. Department of Population Ecology, Friedrich Schiller University Jena, Jena, Germany;3. Department of Ecology and Genetics, Uppsala University, Uppsala, Sweden;4. Institute of Clinical Molecular Biology, Christian‐Albrechts‐University, Kiel, Germany;5. Department of Biological Sciences, Macquarie University, Sydney, NSW, Australia;6. School of Biological, Earth & Environmental Sciences, University of New South Wales, Sydney, NSW, Australia
Abstract:Identifying causal genetic variants underlying heritable phenotypic variation is a long‐standing goal in evolutionary genetics. We previously identified several quantitative trait loci (QTL) for five morphological traits in a captive population of zebra finches (Taeniopygia guttata) by whole‐genome linkage mapping. We here follow up on these studies with the aim to narrow down on the quantitative trait variants (QTN) in one wild and three captive populations. First, we performed an association study using 672 single nucleotide polymorphisms (SNPs) within candidate genes located in the previously identified QTL regions in a sample of 939 wild‐caught zebra finches. Then, we validated the most promising SNP–phenotype associations (n = 25 SNPs) in 5228 birds from four populations. Genotype–phenotype associations were generally weak in the wild population, where linkage disequilibrium (LD) spans only short genomic distances. In contrast, in captive populations, where LD blocks are large, apparent SNP effects on morphological traits (i.e. associations) were highly repeatable with independent data from the same population. Most of those SNPs also showed significant associations with the same trait in other captive populations, but the direction and magnitude of these effects varied among populations. This suggests that the tested SNPs are not the causal QTN but rather physically linked to them, and that LD between SNPs and causal variants differs between populations due to founder effects. While the identification of QTN remains challenging in nonmodel organisms, we illustrate that it is indeed possible to confirm the location and magnitude of QTL in a population with stable linkage between markers and causal variants.
Keywords:association study  genotype–  phenotype maps  linkage mapping  morphology  quantitative trait locus  standing genetic variation
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