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Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [bisulfite-seq]

ABSTRACT: Early mammalian development is accompanied by a profound global remodeling of chromatin-based regulation. The Zdbf2 locus provides a valuable model to uncover the effect of dynamic chromatin transition, as it is polycomb silenced in embryonic stem cells (ESCs) and only becomes activated after Long isoform of Zdbf2 (Liz) transcription-dependent de novo DNA methylation during differentiation. Here we show that four enhancers contribute to the Liz-to-Zdbf2 promoter switch, concomitantly with dynamic changes in chromatin architecture. CTCF plays a key role in partitioning the locus in ESCs, when Liz is active and Zdbf2 is silenced. The partition is relieved when Zdbf2 becomes DNA methylated and active. Mutant ESCs that lack the partition fail to properly activate Zdbf2. Notably, the CTCF-based regulation occurs independently of the polycomb and DNA methylation pathways, suggesting a multi-layered regulatory framework that ensures proper epigenetic programming of a developmentally important gene.

ORGANISM(S): Mus musculus

PROVIDER: GSE121402 | GEO | 2019/04/18

REPOSITORIES: GEO

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Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [ATAC-Seq]

Project description:Early mammalian development is accompanied by a profound global remodeling of chromatin-based regulation. The Zdbf2 locus provides a valuable model to uncover the effect of dynamic chromatin transition, as it is polycomb silenced in embryonic stem cells (ESCs) and only becomes activated after Long isoform of Zdbf2 (Liz) transcription-dependent de novo DNA methylation during differentiation. Here we show that four enhancers contribute to the Liz-to-Zdbf2 promoter switch, concomitantly with dynamic changes in chromatin architecture. CTCF plays a key role in partitioning the locus in ESCs, when Liz is active and Zdbf2 is silenced. The partition is relieved when Zdbf2 becomes DNA methylated and active. Mutant ESCs that lack the partition fail to properly activate Zdbf2. Notably, the CTCF-based regulation occurs independently of the polycomb and DNA methylation pathways, suggesting a multi-layered regulatory framework that ensures proper epigenetic programming of a developmentally important gene.

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Liz transcription is required for evicting H3K27me3 marks at the Gpr1/Zdbf2 locus through the deposition of DNA methylation marks.

Project description:To study the role of the Liz transcript on local chromatin features during early development, we used a culture-based system. Mouse embryonic stem cells (ESCs) with a hypomethylated genome were obtained through their culture in 2i medium supplemented with vitamin C. To recapitulate de novo DNA methylation, these cells were directed towards an epiblast-like cell fate (EpiLC) during seven days of culture in Activin A and Fgf2. The effect of Liz transcription on the maintenance of H3K27me3 marks at the Gpr1/Zdbf2 locus was inferred by the comparative ChIP-seq analysis of H3K27me3 enrichment in WT (E14) cells versus ∆Liz cells- which carry a TALEN-engineered 1.7kb homozygous deletion of the Liz Transcription Start Size (TSS)- at Day 0 (D0), D4 and D7 of EpiLC differentiation.

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Project description:The essential histone variant H2A.Z localises to both active and silent chromatin sites. In embryonic stem cells (ESCs), H2A.Z is also reported to co-localise with polycomb repressive complex 2 (PRC2) at developmentally silenced genes. The mechanism of H2A.Z targeting is not clear, but a role for the PRC2 component Suz12 has been suggested. Given this association, we wished to determine if polycomb functionally directs H2A.Z incorporation in ESCs. We demonstrate that the PRC1 component Ring1B interacts with multiple complexes in ESCs. Moreover, we show that although the genomic distribution of H2A.Z co-localises with PRC2, Ring1B and with the presence of CpG islands, H2A.Z still blankets polycomb target loci in the absence of Suz12, Eed (PRC2) or Ring1B (PRC1). Therefore we conclude that H2A.Z accumulates at developmentally silenced genes in ESCs in a polycomb independent manner. Array design includes 2 biological replicates for all samples and technical replication (dye swaps for H3K27me3_WT_ES, EZH2_WT_ES, EZH2_RING1b_KO_ES, H2AZ_WT_ES(2), H2AZ_Eed_KO_ES and H2AZ_Suz12_KO_ES). Ring1B_WT_ES is represented by a single replicate.

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Chip-chip from WT and Polycomb Component Knock Out Mouse ES cells for H2AZ, H3K27me3, EZH2 and Ring1B.

2012-04-16 | GSE36999 | GEO

Targeted DNA methylation analysis of the imprinted loci FAM50B and ZDBF2 in a cohort of small for gestational age born children

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2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress

Removable insulator facilitates higher-order chromatin remodeling and selective gene expression in the HOXA locus via the retinoic acid signaling [ChIP-chip]

Project description:Chromatin insulators partition the genome into the functional units to control gene expression especially in complex chromosomal regions. The CCCTC-binding factor (CTCF) is an insulator-binding protein which functions for transcriptional regulation and higher-order chromatin formation. Here we report that a removable CTCF insulator is responsible for the retinoic acid (RA)-mediated higher-order chromatin remodeling and selective gene expression in the human HOXA gene locus. Our detailed chromatin analyses characterized multiple CTCF-enriched sites and RA-responsive enhancers in this locus. These regulatory elements and transcriptionally silent HOXA genes were closely positioned under the basal condition. Notably, upon the RA signaling, the transcription factor RAR/RXR induced the loss of an adjacent CTCF binding and changed the higher-order chromatin conformation of the overall locus, establishing transcriptionally active, poised and repressive domains that were separated by stably localizing CTCF insulators. This study uncovers that removable insulator spatiotemporally switches higher-order chromatin and multiple gene activities at the chromosomal domain levels, via the cooperation of CTCF and key transcription factors.

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