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Nat Commun. 2015 May 8;6:7030. doi: 10.1038/ncomms8030.

Expression of the vault RNA protects cells from undergoing apoptosis.

Author information

1
Division of Genomics and RNomics, Medical University Innsbruck, Innsbruck A-6020, Austria.
2
1] Division of Genomics and RNomics, Medical University Innsbruck, Innsbruck A-6020, Austria [2] Department of Chemistry and Biochemistry, University of Bern, Bern CH-3012, Switzerland [3] Graduate School for Cellular and Biomedical Sciences, University of Bern Bern 3012, Switzerland.
3
Division of Developmental Immunology, Medical University Innsbruck, Innsbruck A-6020, Austria.
4
1] Research Unit Gene Vectors, Helmholtz Zentrum München, München D-81377, Germany [2] German Center for Infection Research (DZIF), Partner site Munich, München D-81377, Germany.
5
1] Division of Genomics and RNomics, Medical University Innsbruck, Innsbruck A-6020, Austria [2] Department of Chemistry and Biochemistry, University of Bern, Bern CH-3012, Switzerland.

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.

PMID:
25952297
PMCID:
PMC4430821
DOI:
10.1038/ncomms8030
[Indexed for MEDLINE]
Free PMC Article

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