Jiang Zhihua, Michal Jennifer J, Chen Jie, Daniels Tyler F, Kunej Tanja, Garcia Matthew D, Gaskins Charles T, Busboom Jan R, Alexander Leeson J, Wright Raymond W, Macneil Michael D
Department of Animal Sciences, Washington State University, Pullman, WA 99164-6351, USA.
Int J Biol Sci. 2009 Jul 29;5(6):528-42. doi: 10.7150/ijbs.5.528.
Quantitative or complex traits are determined by the combined effects of many loci, and are affected by genetic networks or molecular pathways. In the present study, we genotyped a total of 138 mutations, mainly single nucleotide polymorphisms derived from 71 functional genes on a Wagyu x Limousin reference population. Two hundred forty six F(2) animals were measured for 5 carcass, 6 eating quality and 8 fatty acid composition traits. A total of 2,280 single marker-trait association runs with 120 tagged mutations selected based on the HAPLOVIEW analysis revealed 144 significant associations (P < 0.05), but 50 of them were removed from the analysis due to the small number of animals (< or = 9) in one genotype group or absence of one genotype among three genotypes. The remaining 94 single-trait associations were then placed into three groups of quantitative trait modes (QTMs) with additive, dominant and overdominant effects. All significant markers and their QTMs associated with each of these 19 traits were involved in a linear regression model analysis, which confirmed single-gene associations for 4 traits, but revealed two-gene networks for 8 traits and three-gene networks for 5 traits. Such genetic networks involving both genotypes and QTMs resulted in high correlations between predicted and actual values of performance, thus providing evidence that the classical Mendelian principles of inheritance can be applied in understanding genetic complexity of complex phenotypes. Our present study also indicated that carcass, eating quality and fatty acid composition traits rarely share genetic networks. Therefore, marker-assisted selection for improvement of one category of these traits would not interfere with improvement of another.
数量性状或复杂性状由许多基因座的综合效应决定,并受遗传网络或分子途径影响。在本研究中,我们对一个和牛×利木赞参考群体中总共138个突变进行了基因分型,这些突变主要是来自71个功能基因的单核苷酸多态性。对246头F(2)代动物的5个胴体性状、6个肉质性状和8个脂肪酸组成性状进行了测量。基于HAPLOVIEW分析选择的120个标签突变进行了总共2280次单标记-性状关联分析,共揭示了144个显著关联(P < 0.05),但其中50个因一个基因型组中的动物数量少(≤9头)或三种基因型中缺少一种基因型而被排除在分析之外。然后将其余94个单性状关联分为具有加性、显性和超显性效应的三组数量性状模式(QTMs)。与这19个性状中的每一个相关的所有显著标记及其QTMs都参与了线性回归模型分析,该分析确认了4个性状的单基因关联,但揭示了8个性状的双基因网络和5个性状的三基因网络。这种涉及基因型和QTMs的遗传网络导致了性能预测值与实际值之间的高度相关性,从而提供了证据表明经典的孟德尔遗传原理可用于理解复杂表型的遗传复杂性。我们目前的研究还表明,胴体、肉质和脂肪酸组成性状很少共享遗传网络。因此,针对这些性状中的一类进行标记辅助选择不会干扰另一类性状的改良。