Proteomic analysis of murine Piwi proteins reveals a role for arginine methylation in specifying interaction with Tudor family members

  1. Vasily V. Vagin1,
  2. James Wohlschlegel2,
  3. Jun Qu3,
  4. Zophonias Jonsson2,
  5. Xinhua Huang2,
  6. Shinichiro Chuma4,
  7. Angelique Girard1,
  8. Ravi Sachidanandam5,
  9. Gregory J. Hannon1,6 and
  10. Alexei A. Aravin1,7
  1. 1Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA;
  2. 2Department of Biological Chemistry, University of California at Los Angeles, Los Angeles, California 90095, USA;
  3. 3Department of Pharmaceutical Sciences, State University of New York at Buffalo and New York State Center of Excellence in Bioinformatics and Life Sciences, Buffalo, New York 14203, USA;
  4. 4Department of Development and Differentiation, Institute for Frontier Medical Sciences, Kyoto University, Shogoin, Sakyo-ku, Kyoto 606-8507 Japan;
  5. 5Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA

    Abstract

    In germ cells, Piwi proteins interact with a specific class of small noncoding RNAs, piwi-interacting RNAs (piRNAs). Together, these form a pathway that represses transposable elements, thus safeguarding germ cell genomes. Basic models describe the overall operation of piRNA pathways. However, the protein compositions of Piwi complexes, the critical protein–protein interactions that drive small RNA production and target recognition, and the precise molecular consequences of conserved localization to germline structures, call nuage, remains poorly understood. We purified the three murine Piwi family proteins, MILI, MIWI, and MIWI2, from mouse germ cells and characterized their interacting protein partners. Piwi proteins were found in complex with PRMT5/WDR77, an enzyme that dimethylates arginine residues. By immunoprecipitation with specific antibodies and by mass spectrometry, we found that Piwi proteins are arginine methylated at conserved positions in their N termini. These modifications are essential to direct complex formation with specific members of the Tudor protein family. Recognition of methylarginine marks by Tudor proteins can drive the localization of Piwi proteins to cytoplasmic foci in an artificial setting, supporting a role for this interaction in Piwi localization to nuage, a characteristic that correlates with proper operation of the piRNA pathway and transposon silencing in multiple organisms.

    Keywords

    Footnotes

    • 6 Corresponding authors.

      E-MAIL hannon{at}cshl.edu; FAX (516) 367-8874.

    • 7 E-MAIL aravin{at}cshl.edu; FAX (516) 367-8874.

    • Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.1814809.

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

      • Received April 24, 2009.
      • Accepted June 8, 2009.
    • Freely available online through the Genes & Development Open Access option.

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