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Elife. 2016 Jan 26;5:e11473. doi: 10.7554/eLife.11473.

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

Author information

1
Wellcome Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences, Institute of Biodiversity Animal Health and Comparative Medicine, University of Glasgow, Glasgow, United Kingdom.
2
Sanger Institute, Wellcome Trust Genome Campus, Cambridge, United Kingdom.
3
West Medical Building, Office 350, University of Glasgow, Glasgow, Scotland.
4
UFR Environnement, Laboratoire des Interactions Hôte-Microorganismes-Environnement et Evolution (LIHME), Université Jean Lorougnon GUEDE, Daloa, Côte d'Ivoire.
5
Institut de Recherche pour le Développement, Campus International de Baillarguet, Montpellier, France.
6
Centre International de Recherche-Développement de l'Elevage en zone Subhumide, Bobo-Dioulasso, Burkina Faso.
7
Université Polytechnique de Bobo-Dioulasso, UFR Sciences et Techniques, Bobo-Dioulasso, Burkina Faso.
8
Programme National de Lutte contre la Trypanosomiase Humaine Africaine, Conakry, Guinea.

Abstract

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.

KEYWORDS:

Meselson effect; Trypanosoma brucei gambiense; evolutionary biology; genomics; infectious disease; microbiology; population genomics; trypanosomiasis

PMID:
26809473
PMCID:
PMC4739771
DOI:
10.7554/eLife.11473
[Indexed for MEDLINE]
Free PMC Article

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