MBE Advance Access published online on July 13, 2007
Molecular Biology and Evolution, doi:10.1093/molbev/msm135
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Research Article |
Dissecting Linkage Disequilibrium in African American Genomes: Roles of Markers and Individuals
1 MOE Key Laboratory of Contemporary Anthropology and Center for Evolutionary Biology, School of Life Sciences and Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, China
2 CAS-MPG Partner Institute of Computational Biology, SIBS, CAS, Shanghai 200031, China
3 Chinese National Human Genome Center at Shanghai 201203, China
4 Rui Jin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China
5 Human Genetics Center, School of Public Health, University of Texas-Health Science Center at Houston, Houston, TX 77225, USA
Address for correspondence and reprints: Dr. Li Jin, Institute of Genetics, School of Life Sciences at Fudan University, 220 Handan Road, Shanghai, China, 200433. E-mail: ljin007{at}gmail.com
Received for publication April 24, 2007. Revision received June 21, 2007. Revision received June 22, 2007. Accepted for publication June 25, 2007.
Substantial increases of linkage disequilibrium (LD) both in magnitude and in range have been observed in recently admixed populations such as African American (AfA). On the other hand, it has also been shown that LD in African Americans was very similar to that of African. In this study, we attempted to resolve these contradicting observations by conducting a systematic examination of the LD structure in African Americans by genotyping a sample of African American individuals at 24,341 SNPs spanning almost the entire chromosome 21, with an average density of 1.5 kb/SNP. The overall LD in African Americans is similar to that in African populations and much less than that in European populations. Even when the ancestry-informative markers (AIMs) were used, extended LD in AfA was found to be limited to certain magnitude range (0.2
r2 0.8) and certain distance range, i.e between-marker distance (BMD) more than 200 kb. Furthermore, the inclusion of African American individuals with predominantly African ancestry was found to reduce the overall magnitude of LD. Elevation of LD in the African American population, compared with its parental populations, can only be observed at the markers with large allele frequency differences between two parental populations at limited scenario. African American individuals of wholly African ancestry contribute little to the extended LD in the African American population, and further genotyping or association analysis conducted using only admixed individuals may lead to higher statistical power and possibly reduced cost.
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