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Undermethylation associated with retroelement activation and chromosome remodelling in an interspecific mammalian hybrid

Author

Listed:
  • Rachel J. Waugh O'Neill

    (La Trobe University
    Princeton University)

  • Michael J. O'Neill

    (Princeton University)

  • Jennifer A. Marshall Graves

    (La Trobe University)

Abstract

Genetic models1,2 predict that genomic rearrangement in hybrids can facilitate reproductive isolation and the formation of new species by preventing gene flow between the parent species and hybrid (sunflowers are an example3). The mechanism underlying hybridization-induced chromosome remodelling is as yet unknown, although mobile element activity has been shown to be involved in DNA rearrangement in some dysgenic Drosophila hybrids4,5. It has been proposed that DNA methylation evolved as a means of repressing the movement of mobile elements (the host defence model6,7). If such a protective mechanism were to fail, mobile elements could be activated, and could cause major and rapid genome alterations8,9. Here we demonstrate the occurrence of genome-wide undermethylation, retroviral element amplification and chromosome remodelling in an interspecific mammalian hybrid (Macropus eugenii × Wallabia bicolor). Atypically extended centromeres of Macropus eugenii derived autosomes in the hybrid were composed primarily of an unmethylated, amplified retroviral element not detectable in either parent species. These results, taken with the observation of deficient methylation and de novo chromosome change in other mammalian hybrids, indicate that the failure of DNA methylation and subsequent mobile-element activity in hybrids could facilitate rapid karyotypic evolution.

Suggested Citation

  • Rachel J. Waugh O'Neill & Michael J. O'Neill & Jennifer A. Marshall Graves, 1998. "Undermethylation associated with retroelement activation and chromosome remodelling in an interspecific mammalian hybrid," Nature, Nature, vol. 393(6680), pages 68-72, May.
  • Handle: RePEc:nat:nature:v:393:y:1998:i:6680:d:10.1038_29985
    DOI: 10.1038/29985
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