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Mol Cell. 2015 Sep 17;59(6):984-97. doi: 10.1016/j.molcel.2015.07.019. Epub 2015 Aug 27.

PARP1- and CTCF-Mediated Interactions between Active and Repressed Chromatin at the Lamina Promote Oscillating Transcription.

Author information

1
Department of Microbiology, Tumor and Cell Biology, Nobels väg 16, Karolinska Institutet, 17177 Stockholm, Sweden.
2
Department of Biosciences and Nutrition, Novum, Karolinska Institutet, 14183 Huddinge, Sweden.
3
Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 17121 Stockholm, Sweden.
4
Department of Microbiology, Tumor and Cell Biology, Nobels väg 16, Karolinska Institutet, 17177 Stockholm, Sweden; Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, Szigeti út 12, 7624 Pécs, Hungary.
5
Department of Microbiology, Tumor and Cell Biology, Nobels väg 16, Karolinska Institutet, 17177 Stockholm, Sweden. Electronic address: anita.gondor@ki.se.

Abstract

Transcriptionally active and inactive chromatin domains tend to segregate into separate sub-nuclear compartments to maintain stable expression patterns. However, here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains (LADs). The interactome is regulated by PARP1 and its co-factor CTCF. They not only mediate chromatin fiber interactions but also promote the recruitment of circadian genes to the lamina. Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Furthermore, depletion of H3K9me2/3, inhibition of PARP activity by olaparib, or downregulation of PARP1 or CTCF expression counteracts both recruitment to the envelope and circadian transcription. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity.

PMID:
26321255
DOI:
10.1016/j.molcel.2015.07.019
[Indexed for MEDLINE]
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