Drosophila telomeric retrotransposons derived from an ancestral element that was recruited to replace telomerase

  1. Alfredo Villasante1,4,
  2. José P. Abad1,
  3. Rosario Planelló1,3,
  4. María Méndez-Lago1,
  5. Susan E. Celniker2, and
  6. Beatriz de Pablos1
  1. 1 Centro de Biología Molecular “Severo Ochoa” (CSIC-UAM), Cantoblanco, 28049 Madrid, Spain;
  2. 2 Berkeley Drosophila Genome Project, Department of Genome Sciences, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA

Abstract

Drosophila telomeres do not have arrays of simple telomerase-generated G-rich repeats. Instead, Drosophila maintains its telomeres by occasional transposition of specific non-long terminal repeat (non-LTR) retrotransposons to chromosome ends. The genus Drosophila provides a superb model system for comparative telomere analysis. Here we present an evolutionary study of Drosophila telomeric elements to ascertain the significance of telomeric retrotransposons (TRs) in the maintenance of Drosophila telomeres. PCR and in silico surveys in the sibling species of Drosophila melanogaster and in more distantly related species show that multiple TRs maintain telomeres in Drosophila. In addition to TRs with two open reading frames (ORFs) capable of autonomous transposition, there are deleted telomeric retrotransposons that have lost their ORF2, which we refer to as half telomeric-retrotransposons (HTRs). The phylogenetic relationship among these telomeric elements is congruent with the phylogeny of the species, suggesting that they have been vertically inherited from a common ancestor. Our results suggest that an existing non-LTR retrotransposon was recruited to perform the cellular function of telomere maintenance.

Footnotes

  • 3 Present address: Facultad de Ciencias, UNED Senda del Rey 9, 28040 Madrid, Spain.

  • 4 Corresponding author.

    4 E-mail avillasante{at}cbm.uam.es; fax 34-91-4974799.

  • [Supplemental material is available online at www.genome.org. The sequence data from this study have been submitted to GenBank under accession nos. AM161543, AM040250-6, AM040240-1, AM040246-9, and AM040237-9.]

  • Article published online before print. Article and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.6365107

    • Received February 6, 2007.
    • Accepted May 16, 2007.
  • Freely available online through the Genome Research Open Access option.

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