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Nat Commun. 2018 Apr 24;9(1):1636. doi: 10.1038/s41467-018-04100-3.

Long ncRNA A-ROD activates its target gene DKK1 at its release from chromatin.

Author information

1
Max Planck Institute for Molecular Genetics, 14195, Berlin, Germany. ntini@molgen.mpg.de.
2
Max Planck Institute for Molecular Genetics, 14195, Berlin, Germany.
3
Free University Berlin, 14195, Berlin, Germany.
4
Humboldt University, 10115, Berlin, Germany.
5
Max Planck Institute for Molecular Genetics, 14195, Berlin, Germany. ulf.orom@mbg.au.dk.
6
Institute for Molecular Biology and Genetics, Aarhus University, 8000, Aarhus, Denmark. ulf.orom@mbg.au.dk.

Abstract

Long ncRNAs are often enriched in the nucleus and at chromatin, but whether their dissociation from chromatin is important for their role in transcription regulation is unclear. Here, we group long ncRNAs using epigenetic marks, expression and strength of chromosomal interactions; we find that long ncRNAs transcribed from loci engaged in strong long-range chromosomal interactions are less abundant at chromatin, suggesting the release from chromatin as a crucial functional aspect of long ncRNAs in transcription regulation of their target genes. To gain mechanistic insight into this, we functionally validate the long ncRNA A-ROD, which enhances DKK1 transcription via its nascent spliced released form. Our data provide evidence that the regulatory interaction requires dissociation of A-ROD from chromatin, with target specificity ensured within the pre-established chromosomal proximity. We propose that the post-transcriptional release of a subset of long ncRNAs from the chromatin-associated template plays an important role in their function as transcription regulators.

PMID:
29691407
PMCID:
PMC5915440
DOI:
10.1038/s41467-018-04100-3
[Indexed for MEDLINE]
Free PMC Article

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