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Related Experiment Videos

Natural selection on the erythrocyte surface.

Jake Baum1, Ryk H Ward, David J Conway

  • 1Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine. Institute of Biological Anthropology, University of Oxford. jacob.baum@lshtm.ac.uk

Molecular Biology and Evolution
|February 28, 2002
PubMed
Summary

The pathogen decoy hypothesis explains how Glycophorin A (GYPA) on red blood cells evolves. Strong selection drives GYPA changes between species and maintains variation within humans, suggesting a role in pathogen defense.

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Area of Science:

  • Evolutionary biology
  • Genetics
  • Immunology

Background:

  • Surface glycoproteins act as pathogen receptors for cell invasion.
  • Mammalian erythrocyte glycoproteins may function as decoy receptors, diverting pathogens.
  • Glycophorin A (GYPA) is the most abundant erythrocyte sialoglycoprotein with an unknown function.

Purpose of the Study:

  • To investigate the evolutionary pressures on Glycophorin A (GYPA).
  • To test the pathogen decoy hypothesis for GYPA function.
  • To understand GYPA's role in pathogen interactions and human health.

Main Methods:

  • Analysis of gypa sequence variation across six primate species.
  • Examination of gypa polymorphisms within a human population.
  • Statistical analysis to detect signatures of selection (positive and balancing).

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Main Results:

  • Excess of replacement substitutions in primate gypa sequences, particularly in exons 2-4.
  • Significant excess of polymorphisms in human exon 2 of gypa.
  • Both patterns indicate strong positive and balancing selection on GYPA.

Conclusions:

  • The pathogen decoy hypothesis adequately explains the observed evolutionary signatures in GYPA.
  • GYPA's evolution suggests a critical role in defense against pathogens.
  • Understanding GYPA function has implications for erythrocyte roles in health and disease.