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Series GSE63346 Query DataSets for GSE63346
Status Public on Sep 04, 2015
Title Pre-patterning of differentiation-driven nuclear lamin A/C-associated chromatin domains by GlcNAcylated histone H2B
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary Dynamic interactions of nuclear lamins with chromatin through so-called lamin-associated domains (LADs) contribute to spatial arrangements of the genome. Here, we provide evidence for pre-patterning of differentiation-driven formation of lamin A/C LADs by domains of histone H2B modified by the nutrient sensor O-linked N-acetylglucosamine (H2BGlcNAc), which we term GADs. We demonstrate a two-step process of lamin A/C LAD formation during in vitro adipogenesis, involving (i) a spreading of lamin A/C-chromatin interactions during the transition from progenitor cell proliferation to cell cycle arrest, and (ii) a genome-scale redistribution these interactions through a process of LAD ‘exchange’ within hours of adipogenic induction. Chromatin state modeling reveals that lamin A/C LADs can be found both in active and repressive chromatin contexts which can be influenced by cell differentiation status. De novo formation of adipogenic lamin A/C LADs occurs non-randomly on GADs, consisting of megabase-size intergenic and repressive chromatin domains. Accordingly, while pre-differentiation lamin A/C LADs are gene-rich, post-differentiation LADs harbor repressive features reminiscent of lamin B1 LADs. Moreover, release of lamin A/C from genes directly involved in glycolysis concurs with their transcriptional upregulation after adipogenic induction, and with concordant downstream elevations in H2BGlcNAc levels and O-GlcNAc cycling. Our results unveil an epigenetic pre-patterning of adipogenic LADs by GADs, suggesting a coupling of developmentally regulated lamin A/C-genome interactions to a metabolically sensitive chromatin modification.
Overall design Examination of LMNA and H2BGlcNAc binding in ASCs across differentiation
Contributor(s) Shah A, Rønningen T, Oldenburg A, Delbarre E, Moskaug JO, Collas P
Citation(s) 26359231
Submission date Nov 17, 2014
Last update date May 15, 2019
Contact name Philippe Collas
Organization name University of Oslo
Department Institute of Basic Medical Sciences
Street address PO Box 1112 Blindern
City Oslo
ZIP/Postal code 0317
Country Norway
Platforms (1)
GPL16791 Illumina HiSeq 2500 (Homo sapiens)
Samples (12)
GSM1546361 H2BGlcNAc_Day-2
GSM1546362 H2BGlcNAc_Day0
GSM1546363 H2BGlcNAc_Day1
BioProject PRJNA267547
SRA SRP049946

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Supplementary file Size Download File type/resource
GSE63346_RAW.tar 267.2 Mb (http)(custom) TAR (of BED, BW, CSV)
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Raw data are available in SRA
Processed data provided as supplementary file

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