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Population genomics reveals the origin and asexual evolution of human infective trypanosomes
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...
Autores principales: | , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4739771/ https://www.ncbi.nlm.nih.gov/pubmed/26809473 http://dx.doi.org/10.7554/eLife.11473 |
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author | Weir, William Capewell, Paul Foth, Bernardo Clucas, Caroline Pountain, Andrew Steketee, Pieter Veitch, Nicola Koffi, Mathurin De Meeûs, Thierry Kaboré, Jacques Camara, Mamadou Cooper, Anneli Tait, Andy Jamonneau, Vincent Bucheton, Bruno Berriman, Matt MacLeod, Annette |
author_facet | Weir, William Capewell, Paul Foth, Bernardo Clucas, Caroline Pountain, Andrew Steketee, Pieter Veitch, Nicola Koffi, Mathurin De Meeûs, Thierry Kaboré, Jacques Camara, Mamadou Cooper, Anneli Tait, Andy Jamonneau, Vincent Bucheton, Bruno Berriman, Matt MacLeod, Annette |
author_sort | Weir, William |
collection | PubMed |
description | 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. DOI: http://dx.doi.org/10.7554/eLife.11473.001 |
format | Online Article Text |
id | pubmed-4739771 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-47397712016-02-05 Population genomics reveals the origin and asexual evolution of human infective trypanosomes Weir, William Capewell, Paul Foth, Bernardo Clucas, Caroline Pountain, Andrew Steketee, Pieter Veitch, Nicola Koffi, Mathurin De Meeûs, Thierry Kaboré, Jacques Camara, Mamadou Cooper, Anneli Tait, Andy Jamonneau, Vincent Bucheton, Bruno Berriman, Matt MacLeod, Annette eLife Genomics and Evolutionary Biology 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. DOI: http://dx.doi.org/10.7554/eLife.11473.001 eLife Sciences Publications, Ltd 2016-01-26 /pmc/articles/PMC4739771/ /pubmed/26809473 http://dx.doi.org/10.7554/eLife.11473 Text en © 2015, Weir et al http://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Genomics and Evolutionary Biology Weir, William Capewell, Paul Foth, Bernardo Clucas, Caroline Pountain, Andrew Steketee, Pieter Veitch, Nicola Koffi, Mathurin De Meeûs, Thierry Kaboré, Jacques Camara, Mamadou Cooper, Anneli Tait, Andy Jamonneau, Vincent Bucheton, Bruno Berriman, Matt MacLeod, Annette Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title | Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title_full | Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title_fullStr | Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title_full_unstemmed | Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title_short | Population genomics reveals the origin and asexual evolution of human infective trypanosomes |
title_sort | population genomics reveals the origin and asexual evolution of human infective trypanosomes |
topic | Genomics and Evolutionary Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4739771/ https://www.ncbi.nlm.nih.gov/pubmed/26809473 http://dx.doi.org/10.7554/eLife.11473 |
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