LETTER

A Population Threshold for Functional Polymorphisms

    • 1 University of Washington Genome Center, Department of Medicine, Seattle, Washington 98195, USA
    • 2 James Watson Institute of Zhejiang University, Hangzhou Genomics Institute, Key Laboratory of Bioinformatics of Zhejiang Province, Hangzhou 310007, China
    • 3 Beijing Institute of Genomics, Center of Genomics and Bioinformatics, Chinese Academy of Sciences, Beijing 101300, China
    • 4 Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia
    • 5 The Institute of Human Genetics, University of Aarhus, DK-8000 Århus C, Denmark
Published August 5, 2003. Vol 13 Issue 8, pp. 1873-1879. https://doi.org/10.1101/gr.1324303
Download PDF Please log-in to or register for your personal account in order to access PDF Cite Article Permissions Share
cover of Genome Research Vol 36 Issue 4
Current Issue:

Abstract

We sequenced 114 genes (for DNA repair, cell cycle arrest, apoptosis, and detoxification)in a mixed human population and observed a sudden increase in the number of functional polymorphisms below a minor allele frequency of ∼6%. Functionality is assessed by considering the ratio in the number of nonsynonymous single nucletide polymorphisms (SNPs)to the number of synonymous or intron SNPs. This ratio is steady from below 1% in frequency—that regime traditionally associated with rare Mendelian diseases—all the way up to about 6% in frequency, after which it falls precipitously. We consider possible explanations for this threshold effect. There are four candidates as follows: (1)deleterious variants that have yet to be purified from the population, (2)balancing selection, in which a selective advantage accrues to the heterozygotes, (3)population-specific functional polymorphisms, and (4)adaptive variants that are accumulating in the population as a response to the dramatic environmental changes of the last 7,000∼17,000 years.

Loading
Loading
Back to top