Haplotype Diversity and Linkage Disequilibrium at Human G6PD : Recent Origin of Alleles That Confer Malarial Resistance-Reference-Cited by-同舟云学术

Haplotype Diversity and Linkage Disequilibrium at Human G6PD : Recent Origin of Alleles That Confer Malarial Resistance

Published:2001-07-20 Issue:5529 Volume:293 Page:455-462
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Tishkoff Sarah A.¹²,Varkonyi Robert²,Cahinhinan Nelie²,Abbes Salem³,Argyropoulos George⁴,Destro-Bisol Giovanni⁵,Drousiotou Anthi⁶,Dangerfield Bruce⁷,Lefranc Gerard⁸,Loiselet Jacques⁹,Piro Anna¹⁰,Stoneking Mark¹¹,Tagarelli Antonio¹⁰,Tagarelli Giuseppe¹⁰,Touma Elias H.⁹,Williams Scott M.¹²,Clark Andrew G.²

Affiliation:

1. Department of Biology, Biology/Psychology Building, University of Maryland, College Park, MD 20742, USA.

2. Institute of Evolutionary Genetics, Department of Biology, Pennsylvania State University, University Park, PA 16802, USA.

3. Faculty of Medicine and Pasteur Institute, Tunis, Tunisia.

4. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.

5. Department of Human and Animal Biology, University “La Sapienza,” Rome, Italy.

6. Department of Biochemical Genetics, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.

7. Department of Human Genetics, South African Institute of Medical Research, University of the Witwatersrand, Johannesburg, South Africa.

8. University of Sciences and CNRS, Montpellier, France.

9. University St. Joseph, Beirut, Lebanon.

10. Istituto di Medicina Sperimentale e Biotecnologie–CNR, Mangone (Cosenza), Italy.

11. Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.

12. Department of Microbiology, Meharry Medical College, Nashville, TN 37208, USA.

Abstract

The frequencies of low-activity alleles of glucose-6-phosphate dehydrogenase in humans are highly correlated with the prevalence of malaria. These “deficiency” alleles are thought to provide reduced risk from infection by the Plasmodium parasite and are maintained at high frequency despite the hemopathologies that they cause. Haplotype analysis of “A−” and ”Med“ mutations at this locus indicates that they have evolved independently and have increased in frequency at a rate that is too rapid to be explained by random genetic drift. Statistical modeling indicates that the A− allele arose within the past 3840 to 11,760 years and the Med allele arose within the past 1600 to 6640 years. These results support the hypothesis that malaria has had a major impact on humans only since the introduction of agriculture within the past 10,000 years and provide a striking example of the signature of selection on the human genome.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference62 articles.

1. The molecular basis of glucose-6-phosphate dehydrogenase deficiency

2. G6PD deficiency

3. Glucose-6-phosphate dehydrogenase deficiency and malaria

4. L. Luzatto A. Mehta T. Vulliamy in The Metabolic and Molecular Bases of Inherited Disease C. R. Scriver A. L. Beaudet W. S. Sly D. Valle Eds. (McGraw-Hill New York ed. 8 2001) pp. 4517–4553.

5. Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria

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