Bull S B, Pinnaduwage D, Shin J, Xie F, Tritchler D
Department of Preventive Medicine, University of Toronto, Ontario, Canada.
Genet Epidemiol. 1997;14(6):965-70. doi: 10.1002/(SICI)1098-2272(1997)14:6<965::AID-GEPI67>3.0.CO;2-J.
In a randomly chosen replicate of extended pedigrees from GAW10, we conducted robust multipoint genome scans for linkage using a dense marker map. For analysis of the quantitative traits, we selected sibships from the pedigrees, and for analysis of disease status, small families of affected relatives were selected. Lod-score likelihood analyses were conducted in the full pedigrees and in the affected relative families for selected regions. We located a flanking marker for MG1 on chromosome 5, and identified marker regions including MG2, MG4, and MG5 on chromosomes 8 and 9. The analytic methods were consistent for the major gene with a strong effect; false positive errors on chromosomes 1 and 10 could have been eliminated by requiring evidence from more than one method.
在GAW10扩展家系的一个随机选择的重复样本中，我们使用密集标记图谱进行了稳健的多点基因组连锁扫描。对于数量性状分析，我们从家系中选择同胞对；对于疾病状态分析，我们选择受影响亲属的小家庭。在完整家系和选定区域的受影响亲属家庭中进行了Lod分数似然分析。我们在5号染色体上定位了MG1的侧翼标记，并在8号和9号染色体上鉴定了包括MG2、MG4和MG5在内的标记区域。对于具有强效应的主基因，分析方法是一致的；通过要求多种方法提供证据，1号和10号染色体上的假阳性错误本可以消除。
