Templeton A R, Clark A G, Weiss K M, Nickerson D A, Boerwinkle E, Sing C F
Department of Biology, Washington University, St. Louis, MO 63130-4899, USA.
Am J Hum Genet. 2000 Jan;66(1):69-83. doi: 10.1086/302699.
Here an analysis is presented of the roles of recombination and mutation in shaping previously determined haplotype variation in 9.7 kb of genomic DNA sequence from the human lipoprotein lipase gene (LPL), scored in 71 individuals from three populations: 24 African Americans, 24 Finns, and 23 non-Hispanic whites. Recombination and gene-conversion events inferred from data on 88 haplotypes that were defined by 69 variable sites were tested. The analysis revealed 29 statistically significant recombination events and one gene-conversion event. The recombination events were concentrated in a 1.9-kb region, near the middle of the segment, that contains a microsatellite and a pair of tandem and complementary mononucleotide runs; both the microsatellite and the runs show length variation. An analysis of site variation revealed that 9.6% of the nucleotides at CpG sites were variable, as were 3% of the nucleotides found in mononucleotide runs of >/=5 nucleotides, 3% of the nucleotides found </=3 bp from certain putative polymerase alpha-arrest sites, and 0. 5% of the remaining nucleotides. This nonhomogeneous distribution of variation suggests that multiple mutational hits at certain sites are common, an observation that challenges the fundamental assumption of the infinite-sites-mutation model. The nonrandom patterns of recombination and mutation suggest that randomly chosen single-nucleotide polymorphisms may not be optimal for disequilibrium mapping of this gene. Overall, these results indicate that both recombinational and mutational hotspots have played significant roles in shaping the haplotype variation at the LPL locus.
本文对重组和突变在塑造人类脂蛋白脂肪酶基因(LPL)9.7 kb基因组DNA序列中先前确定的单倍型变异所起的作用进行了分析,该序列在来自三个群体的71个人中进行了评分:24名非裔美国人、24名芬兰人和23名非西班牙裔白人。对根据69个可变位点定义的88个单倍型数据推断出的重组和基因转换事件进行了测试。分析发现了29个具有统计学意义的重组事件和1个基因转换事件。重组事件集中在该片段中部附近一个1.9 kb的区域,该区域包含一个微卫星以及一对串联且互补的单核苷酸序列;微卫星和这些序列均显示出长度变异。对位点变异的分析表明,CpG位点处9.6%的核苷酸是可变的,在长度≥5个核苷酸的单核苷酸序列中3%的核苷酸是可变的,在距离某些假定的聚合酶α-阻滞位点≤3 bp处发现的3%的核苷酸是可变的,其余核苷酸中有0.5%是可变的。这种变异的非均匀分布表明,某些位点存在多个突变热点是常见的,这一观察结果挑战了无限位点突变模型的基本假设。重组和突变的非随机模式表明,随机选择的单核苷酸多态性可能并非该基因不平衡定位的最佳选择。总体而言,这些结果表明,重组热点和突变热点在塑造LPL基因座的单倍型变异中都发挥了重要作用。