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Antagonistic coevolution accelerates molecular evolution

机译：拮抗协同进化加速分子进化

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摘要

The Red Queen hypothesis proposes that coevolution of interacting species (such as hosts and parasites) should drive molecular evolution through continual natural selection for adaptation and counter-adaptation. Although the divergence observed at some host-resistance and parasite-infectivity genes is consistent with this, the long time periods typically required to study coevolution have so far prevented any direct empirical test. Here we show, using experimental populations of the bacterium Pseudomonas fluorescens SBW25 and its viral parasite, phage Φ2 (refs 10, 11), that the rate of molecular evolution in the phage was far higher when both bacterium and phage coevolved with each other than when phage evolved against a constant host genotype. Coevolution also resulted in far greater genetic divergence between replicate populations, which was correlated with the range of hosts that coevolved phage were able to infect. Consistent with this, the most rapidly evolving phage genes under coevolution were those involved in host infection. These results demonstrate, at both the genomic and phenotypic level, that antagonistic coevolution is a cause of rapid and divergent evolution, and is likely to be a major driver of evolutionary change within species.
机译：红色女王假说提出，相互作用物种（例如宿主和寄生虫）的共同进化应通过对适应和反适应的持续自然选择来驱动分子进化。尽管在某些宿主抗性基因和寄生虫感染性基因上观察到的差异与此相符，但到目前为止，研究协同进化通常需要较长的时间，从而阻止了任何直接的经验检验。在这里，我们显示，利用荧光假单胞菌SBW25及其病毒寄生物噬菌体Φ2（参考文献10、11）的实验种群，当细菌和噬菌体相互进化时，噬菌体中的分子进化速率远高于噬菌体针对恒定的宿主基因型进化。共同进化还导致复制种群之间的遗传差异更大，这与共同进化的噬菌体能够感染的宿主范围有关。与此相一致，共同进化下进化最快的噬菌体基因是那些参与宿主感染的基因。这些结果在基因组和表型水平上均表明，拮抗协同进化是快速和发散进化的原因，并且可能是物种内进化变化的主要驱动力。

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  • 来源
    《Nature》 |2010年第7286期|275-278|共4页
  • 作者

    Steve Paterson; Tom Vogwill; Angus Buckling; Rebecca Benmayor; Andrew J. Spiers; Nicholas R. Thomson; Mike Quail; Frances Smith; Danielle Walker; Ben Libberton; Andrew Fenton; Neil Hall; Michael A. Brockhurst;

  • 作者单位

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

    Zoology Department, University of Oxford, South Parks Road, Oxford 0X1 3PS, UK;

    Zoology Department, University of Oxford, South Parks Road, Oxford 0X1 3PS, UK;

    SIMBIOS Centre, Level 5 Kydd Building, University of Abertay Dundee, Bell Street, Dundee DD1 1HG, UK;

    Pathogen Genomics, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK;

    Pathogen Genomics, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK;

    Pathogen Genomics, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK;

    Pathogen Genomics, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK;

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

    School of Biological Sciences, Biosciences Building, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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