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Published online before print January 14, 2003, 10.1101/gr.302003
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Vol 13, Issue 2, 173-181, February 2003

Linkage Disequilibrium and Haplotype Diversity in the Genes of the Renin–Angiotensin System: Findings From the Family Blood Pressure Program

Xiaofeng Zhu1,4,5, Denise Yan2,4, Richard S. Cooper1, Amy Luke1, Morna A. Ikeda2, Yen-Pei C. Chang2, Alan Weder3 and Aravinda Chakravarti2

1Department of Preventive Medicine and Epidemiology, Loyola Stritch School of Medicine, Maywood, Illinois 60153, USA;2 McKusick–Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, Maryland 21287, USA; 3Division of Hypertension, University of Michigan School of Medicine, Ann Arbor, Michigan 48109, USA

Association studies of candidate genes with complex traits have generally used one or a few single nucleotide polymorphisms (SNPs), although variation in the extent of linkage disequilibrium (LD) within genes markedly influences the sensitivity and precision of association studies. The extent of LD and the underlying haplotype structure for most candidate genes are still unavailable. We sampled 193 blacks (African-Americans) and 160 whites (European-Americans) and estimated the intragenic LD and the haplotype structure in four genes of the renin–angiotensin system. We genotyped 25 SNPs, with all but one of the pairs spaced between 1 and 20 kb, thus providing resolution at small scale. The pattern of LD within a gene was very heterogeneous. Using a robust method to define haplotype blocks, blocks of limited haplotype diversity were identified at each locus; between these blocks, LD was lost owing to the history of recombination events. As anticipated, there was less LD among blacks, the number of haplotypes was substantially larger, and shorter haplotype segments were found, compared with whites. These findings have implications for candidate-gene association studies and indicate that variation between populations of European and African origin in haplotype diversity is characteristic of most genes.

[The sequence data described in this paper are available in GenBank under the following accession nos: AGT, MIM 106150; Renin, MIM 179820; ACE, MIM 106180; Angiotensin receptor I, MIM 106165. Supplementary material is available online at http://www.genome.org.]

4 These authors contributed equally to this work.

5 Corresponding author.

E-MAIL xzhu1{at}lumc.edu; FAX (708) 327-9009.

Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.302003. Article published online before print in January 2003.


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