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Mol Cell. 2014 Feb 6;53(3):393-406. doi: 10.1016/j.molcel.2014.01.009.

Long noncoding RNA NEAT1-dependent SFPQ relocation from promoter region to paraspeckle mediates IL8 expression upon immune stimuli.

Author information

1
Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
2
Radioisotope Centre, The University of Tokyo, Tokyo 113-0032, Japan.
3
Department of Infection Biology, Faculty of Medicine & Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 305-8575, Japan.
4
Division of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
5
Laboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
6
Department of Bioscience and Bioinformatics, Kyushu Institute of Technology Fukuoka 820-8502, Japan.
7
Department of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Chiba 277-8562, Japan.
8
Department of Chemistry, School of Science, The University of Tokyo, Tokyo 113-0033, Japan.
9
Laboratory for Systems Biology and Medicine, Research Centre for Advanced Science and Technology, The University of Tokyo, Tokyo 153-8904, Japan.
10
Radioisotope Centre, The University of Tokyo, Tokyo 113-0032, Japan; Laboratory for Systems Biology and Medicine, Research Centre for Advanced Science and Technology, The University of Tokyo, Tokyo 153-8904, Japan.
11
Radioisotope Centre, The University of Tokyo, Tokyo 113-0032, Japan. Electronic address: akimitsu@ric.u-tokyo.ac.jp.

Erratum in

  • Mol Cell. 2014 Jun 19;54(6):1055.

Abstract

Although thousands of long noncoding RNAs (lncRNAs) are localized in the nucleus, only a few dozen have been functionally characterized. Here we show that nuclear enriched abundant transcript 1 (NEAT1), an essential lncRNA for the formation of nuclear body paraspeckles, is induced by influenza virus and herpes simplex virus infection as well as by Toll-like receptor3-p38 pathway-triggered poly I:C stimulation, resulting in excess formation of paraspeckles. We found that NEAT1 facilitates the expression of antiviral genes including cytokines such as interleukin-8 (IL8). We found that splicing factor proline/glutamine-rich (SFPQ), a NEAT1-binding paraspeckle protein, is a repressor of IL8 transcription, and that NEAT1 induction relocates SFPQ from the IL8 promoter to the paraspeckles, leading to transcriptional activation of IL8. Together, our data show that NEAT1 plays an important role in the innate immune response through the transcriptional regulation of antiviral genes by the stimulus-responsive cooperative action of NEAT1 and SFPQ.

PMID:
24507715
DOI:
10.1016/j.molcel.2014.01.009
[Indexed for MEDLINE]
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