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Population genomics reveals the origin and asexual evolution of human infective trypanosomes

Research output: Contribution to journalArticle

  • William Weir
  • Paul Capewell
  • Bernardo Foth
  • Caroline Clucas
  • Andrew Pountain
  • Pieter Steketee
  • Nicola Veitch
  • Mathurin Koffi
  • Thierry De Meeûs
  • Jacques Kaboré
  • Mamadou Camara
  • Anneli Cooper
  • Andy Tait
  • Vincent Jamonneau
  • Bruno Bucheton
  • Matt Berriman
  • Annette MacLeod

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    Rights statement: Copyright Weir et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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    Licence: Creative Commons: Attribution (CC-BY)

Original languageEnglish
Publication statusPublished - 26 Jan 2016


Evolutionary theory predicts that the lack of recombination and chromosomal re-assortment in strictly asexual organisms results in homologous chromosomes irreversibly accumulating mutations and thus evolving independently of each other, a phenomenon termed the Meselson effect. We apply a population genomics approach to examine this effect in an important human pathogen, Trypanosoma brucei gambiense. We determine that T.b. gambiense is evolving strictly asexually and is derived from a single progenitor, which emerged within the last 10,000 years. We demonstrate the Meselson effect for the first time at the genome-wide level in any organism and show large regions of loss of heterozygosity, which we hypothesise to be a short-term compensatory mechanism for counteracting deleterious mutations. Our study sheds new light on the genomic and evolutionary consequences of strict asexuality, which this pathogen uses as it exploits a new biological niche, the human population.

    Research areas

  • Evolution, Molecular, Humans, Metagenomics, Mutation, Reproduction, Asexual, Trypanosoma brucei gambiense/genetics, Trypanosomiasis/parasitology

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