Comment on "Ongoing Adaptive Evolution of ASPM, a Brain Size Determinant in Homo sapiens"
Fuli Yu1,2,
R. Sean Hill2,3,4,
Stephen F. Schaffner2,
Pardis C. Sabeti2,
Eric T. Wang5,6,
Andre A. Mignault1,
Russell J. Ferland3,4,
Robert K. Moyzis5,6,
Christopher A. Walsh2,3,4 and
David Reich1,2*
1 Department of Genetics, Harvard Medical School, New Research Building, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
2 Broad Institute of Harvard and MIT, 7 Cambridge Center, Cambridge, MA 02142, USA.
3 Division of Neurogenetics and Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
4 Division of Genetics, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
5 Department of Biological Chemistry, College of Medicine, University of California, Irvine, CA 92697, USA.
6 Institute of Genomics and Bioinformatics, University of California, Irvine, CA 92697, USA.
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Fig. 1. Linkage disequilibrium decay around A44871G in European Americans. (A) Haplotype frequency in European Americans (CEU). Blue bars are the derived haplotypes marked by the G allele. (B) Decay of extended haplotype homozygosity (EHH) around A44871G. (C) The significance of the LRH test at each marker is evaluated empirically by comparing with the genome-wide data from HapMap, matched with regard to breakdown of homozygosity. The most extreme P value of 0.03 is not striking when compared against the lowest P value seen in 1000 comparison regions, 90% of which show stronger evidence for selection at some distance. (D) The extent of the haplotype around the G allele (red dot, defined as the span for which EHH > 0.35), in comparison with alleles of matched frequency in CEU from HapMap on chromosome 1. This is well within the 95% central range of HapMap, whether plotted by physical distance (this figure) or genetic distance (fig. S3). To match the marker density of HapMap Phase I, we randomly dropped SNPs from ASPM until we had 1 SNP every 5 kb. With this lower density, the span of the G haplotype is 285 kb.
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