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  • Invited speaker presentation
  • Open Access

Silencing of retroviruses by small RNAs in Drosophila

  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Retrovirology20096 (Suppl 2) :I4

https://doi.org/10.1186/1742-4690-6-S2-I4

  • Published:

Keywords

  • Transposable Element
  • Small RNAs
  • Host Locus
  • Drosophila Genome
  • Silence Mechanism

Retroviruses propagate also in invertebrates. The Drosophila genome contains many proviruses belonging to several families of endogenous retroviruses. These proviruses are usually repressed, but the mechanisms involved in their repression have been a mystery for a long time.

Gypsy is a Drosophila endogenous retrovirus that is also infectious. Therefore it can propagate both horizontally as infectious retroviruses and vertically as endogenous retroviruses. It can transpose as well as retrotransposons. One of the principal ways of propagation of gypsy involves infection of the female germline by particles produced by somatic cells of the ovaries. This process is normally repressed by the host locus flamenco (flam). Restrictive flam alleles repress gypsy in these somatic cells. We have shown that the repression correlates with the amount of complementary 24-29 nucleotide long piRNAs (Piwi interacting RNAs). These small RNAs are responsible for the control of transposable elements. The silencing mechanisms associated with them are different from the mechanisms associated with siRNAs and miRNAs and have still to be elucidated.

The amount of gypsy piRNAs is determined by the flam locus in a provirus copy number-independent manner and their production is triggered by pericentromeric defective proviruses located in the locus. flam also controls other retroelements. The flam region is very rich in defective copies of retrotransposons and endogenous retroviruses, including gypsy.

Our results indicate that the piRNA silencing pathway may be considered as a sort of immunity system using the defective proviruses (or transposable elements) located in heterochromatin as a repertory directing the silencing machinery toward the transcripts of the corresponding functional retroviruses (or transposable elements).

Authors’ Affiliations

(1)
Institut de Génétique Humaine, CNRS, 34396 Montpellier, France

Copyright

© Brun et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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