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

Evgenia Ntini (), Annita Louloupi, Julia Liz, Jose M. Muino, Annalisa Marsico and Ulf Andersson Vang Ørom ()
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Evgenia Ntini: Max Planck Institute for Molecular Genetics
Annita Louloupi: Max Planck Institute for Molecular Genetics
Julia Liz: Max Planck Institute for Molecular Genetics
Jose M. Muino: Humboldt University
Annalisa Marsico: Max Planck Institute for Molecular Genetics
Ulf Andersson Vang Ørom: Max Planck Institute for Molecular Genetics

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-04100-3

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