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Expression of the vault RNA protects cells from undergoing apoptosis

Author

Listed:
  • Melanie Amort

    (Medical University Innsbruck)

  • Birgit Nachbauer

    (Medical University Innsbruck
    University of Bern
    Graduate School for Cellular and Biomedical Sciences, University of Bern)

  • Selma Tuzlak

    (Medical University Innsbruck)

  • Arnd Kieser

    (Research Unit Gene Vectors, Helmholtz Zentrum München
    German Center for Infection Research (DZIF), Partner site Munich)

  • Aloys Schepers

    (Research Unit Gene Vectors, Helmholtz Zentrum München
    German Center for Infection Research (DZIF), Partner site Munich)

  • Andreas Villunger

    (Medical University Innsbruck)

  • Norbert Polacek

    (Medical University Innsbruck
    University of Bern)

Abstract

Non-protein-coding RNAs are a functionally versatile class of transcripts exerting their biological roles on the RNA level. Recently, we demonstrated that the vault complex-associated RNAs (vtRNAs) are significantly upregulated in Epstein–Barr virus (EBV)-infected human B cells. Very little is known about the function(s) of the vtRNAs or the vault complex. Here, we individually express latent EBV-encoded proteins in B cells and identify the latent membrane protein 1 (LMP1) as trigger for vtRNA upregulation. Ectopic expression of vtRNA1-1, but not of the other vtRNA paralogues, results in an improved viral establishment and reduced apoptosis, a function located in the central domain of vtRNA1-1. Knockdown of the major vault protein has no effect on these phenotypes revealing that vtRNA1-1 and not the vault complex contributes to general cell death resistance. This study describes a NF-κB-mediated role of the non-coding vtRNA1-1 in inhibiting both the extrinsic and intrinsic apoptotic pathways.

Suggested Citation

  • Melanie Amort & Birgit Nachbauer & Selma Tuzlak & Arnd Kieser & Aloys Schepers & Andreas Villunger & Norbert Polacek, 2015. "Expression of the vault RNA protects cells from undergoing apoptosis," Nature Communications, Nature, vol. 6(1), pages 1-11, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8030
    DOI: 10.1038/ncomms8030
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