Telomere elongation is under the control of the RNAi-based mechanism in the Drosophila germline

  1. Mikhail Savitsky1,4,
  2. Dmitry Kwon2,3,
  3. Pavel Georgiev1,
  4. Alla Kalmykova2,5, and
  5. Vladimir Gvozdev2,6
  1. 1Department of the Control of Genetic Processes, Institute of Gene Biology, Russian Academy of Sciences, Moscow 119334, Russia; 2Department of Molecular Genetics of Cell, Institute of Molecular Genetics, Russian Academy of Sciences, Moscow 123182, Russia; 3Department of Molecular Biology, Moscow State University, Moscow 119899, Russia; 4Centre for Medical Studies of Oslo University, Moscow 199334, Russia

Abstract

Telomeres in Drosophila are maintained by transposition of specialized telomeric retroelements HeT-A, TAHRE, and TART instead of the short DNA repeats generated by telomerase in other eukaryotes. Here we implicate the RNA interference machinery in the control of Drosophila telomere length in ovaries. The abundance of telomeric retroelement transcripts is up-regulated owing to mutations in the spn-E and aub genes, encoding a putative RNA helicase and protein of the Argonaute family, respectively, which are related to the RNA interference (RNAi) machinery. These mutations cause an increase in the frequency of telomeric element retrotransposition to a broken chromosome end. spn-E mutations eliminate HeT-A and TART short RNAs in ovaries, suggesting an RNAi-based mechanism in the control of telomere maintenance in the Drosophila germline. Enhanced frequency of TART, but not HeT-A, attachments in individuals carrying one dose of mutant spn-E or aub alleles suggests that TART is a primary target of the RNAi machinery. At the same time, we detected enhanced HeT-A attachments to broken chromosome ends in oocytes from homozygous spn-E mutants. Double-stranded RNA (dsRNA)-mediated control of telomeric retroelement transposition may occur at premeiotic stages, resulting in the maintenance of appropriate telomere length in gamete precursors.

Keywords

Footnotes

  • Supplemental material is available at http://www.genesdev.org.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.370206.

  • Corresponding authors.

  • 5 E-MAIL allakalm{at}img.ras.ru; FAX 7-095-1960221.

  • 6 E-MAIL gvozdev{at}img.ras.ru; FAX 7-095-1960221.

    • Accepted December 1, 2005.
    • Received October 13, 2005.
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