The exon junction complex controls transposable element activity by ensuring faithful splicing of the piwi transcript

  1. Jean-Yves Roignant3
  1. 1Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, Department of Cell Biology, New York University School of Medicine, New York, New York 10016, USA;
  2. 2Howard Hughes Medical Institute,
  3. 3Institute of Molecular Biology (IMB), 55128 Mainz, Germany;
  4. 4Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA
  1. Corresponding author: j.roignant{at}imb-mainz.de
  1. 5 These authors contributed equally to this work.

Abstract

The exon junction complex (EJC) is a highly conserved ribonucleoprotein complex that binds RNAs during splicing and remains associated with them following export to the cytoplasm. While the role of this complex in mRNA localization, translation, and degradation has been well characterized, its mechanism of action in splicing a subset of Drosophila and human transcripts remains to be elucidated. Here, we describe a novel function for the EJC and its splicing subunit, RnpS1, in preventing transposon accumulation in both Drosophila germline and surrounding somatic follicle cells. This function is mediated specifically through the control of piwi transcript splicing, where, in the absence of RnpS1, the fourth intron of piwi is retained. This intron contains a weak polypyrimidine tract that is sufficient to confer dependence on RnpS1. Finally, we demonstrate that RnpS1-dependent removal of this intron requires splicing of the flanking introns, suggesting a model in which the EJC facilitates the splicing of weak introns following its initial deposition at adjacent exon junctions. These data demonstrate a novel role for the EJC in regulating piwi intron excision and provide a mechanism for its function during splicing.

Keywords

Footnotes

  • Received May 19, 2014.
  • Accepted July 15, 2014.

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