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Parallel evolution of domesticated Caenorhabditis species targets pheromone receptor genes

Author

Listed:
  • Patrick T. McGrath

    (Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University)

  • Yifan Xu

    (Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University)

  • Michael Ailion

    (University of Utah)

  • Jennifer L. Garrison

    (Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University)

  • Rebecca A. Butcher

    (University of Florida)

  • Cornelia I. Bargmann

    (Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University)

Abstract

When the worms turned If we could return the planet to ancestral conditions, asked the late Stephen Jay Gould, would we get a replay of the same evolutionary movie? Focusing on the simpler case of nematode domestication, McGrath et al. find that two Caenorhabditis elegans lines and Caenorhabditis briggsae, a species separated by some 20 million years from C. elegans, independently accumulated mutations in a conserved set of pheromone receptor genes, thus reducing the worms' natural trend to hibernate in overcrowded conditions. Such convergence in the adaptation process shows that evolution can indeed be quite reproducible, at least under some specific environmental constraints.

Suggested Citation

  • Patrick T. McGrath & Yifan Xu & Michael Ailion & Jennifer L. Garrison & Rebecca A. Butcher & Cornelia I. Bargmann, 2011. "Parallel evolution of domesticated Caenorhabditis species targets pheromone receptor genes," Nature, Nature, vol. 477(7364), pages 321-325, September.
    • Handle: RePEc:nat:nature:v:477:y:2011:i:7364:d:10.1038_nature10378
    DOI: 10.1038/nature10378
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    Cited by:

    1. James S. Horton & Louise M. Flanagan & Robert W. Jackson & Nicholas K. Priest & Tiffany B. Taylor, 2021. "A mutational hotspot that determines highly repeatable evolution can be built and broken by silent genetic changes," Nature Communications, Nature, vol. 12(1), pages 1-10, December.

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