Natural selection on protein-coding genes in the human genome

Carlos D. Bustamante (), Adi Fledel-Alon, Scott Williamson, Rasmus Nielsen, Melissa Todd Hubisz, Stephen Glanowski, David M. Tanenbaum, Thomas J. White, John J. Sninsky, Ryan D. Hernandez, Daniel Civello, Mark D. Adams, Michele Cargill and Andrew G. Clark
Additional contact information
Carlos D. Bustamante: Cornell University
Adi Fledel-Alon: Cornell University
Scott Williamson: Cornell University
Rasmus Nielsen: Cornell University
Melissa Todd Hubisz: Cornell University
Stephen Glanowski: Applied Biosystems
David M. Tanenbaum: Applied Biosystems
Thomas J. White: Celera Diagnostics
John J. Sninsky: Celera Diagnostics
Ryan D. Hernandez: Cornell University
Daniel Civello: Celera Diagnostics
Mark D. Adams: Case Western Reserve University
Michele Cargill: Celera Diagnostics
Andrew G. Clark: Cornell University

Nature, 2005, vol. 437, issue 7062, 1153-1157

Abstract: Go forth and evolve Are we still evolving? The simple answer is yes. A comparison of the sequences of over 11,000 genes from 39 human individuals and from chimpanzees reveals more than 1,139 genes that show evidence of either positive or weak negative selection. Certain gene types (such as transcription factors) show an excess of rapidly evolving genes and others (such as cytoskeletal proteins) show an excess of genes subject to weak negative selection. Genes associated with human disease tend to show a signature of past selection: this may be because complex common diseases are most likely to arise from genes that can tolerate mildly deleterious variation. Mutations that grossly affect gene function are likely to be kept at low frequencies by natural selection and thus contribute little to explaining variation in common disease.

Date: 2005
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DOI: 10.1038/nature04240

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