Palmer L J, Jacobs K B, Scurrah K J, Xu X, Horvath S, Weiss S T
Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio, USA.
Genet Epidemiol. 2001;21 Suppl 1:S674-9. doi: 10.1002/gepi.2001.21.s1.s674.
We used variance components analysis to investigate the underlying determinants of the quantitative phenotypes (Q1-Q5) and their interrelationships in replicate 42 of the Genetic Analysis Workshop 12 simulated general population. Variance components models were fitted using Gibbs sampling in WinBUGS v1.3. Sigma-squared-A-random-effects (SSARs) were estimated for each phenotype, and were used as derived phenotypes in subsequent linkage analyses. Whole-genome, multipoint linkage analyses were based upon a new Haseman-Elston identity-by descent sib-pair method that takes a weighted combination of the trait-sum and trait-difference. The five quantitative traits simulated were closely correlated with each other and with affection status. The whole-genome screen of quantitative traits associated with the simulated complex disease suggested that one or more major loci regulating Q1 localizes to chromosome 2p and that one or more major loci regulating Q5 may localize to chromosome 1p.
我们使用方差成分分析来研究遗传分析研讨会12模拟普通人群的第42次重复中定量表型(Q1 - Q5)的潜在决定因素及其相互关系。使用WinBUGS v1.3中的吉布斯采样拟合方差成分模型。为每个表型估计了西格玛平方A随机效应(SSARs),并将其用作后续连锁分析中的派生表型。全基因组多点连锁分析基于一种新的哈斯曼 - 埃尔斯顿同源等位基因对方法,该方法采用性状总和与性状差异的加权组合。模拟的五个定量性状彼此之间以及与患病状态密切相关。与模拟复杂疾病相关的定量性状的全基因组筛选表明,调节Q1的一个或多个主要基因座定位于2号染色体p臂,调节Q5的一个或多个主要基因座可能定位于1号染色体p臂。