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RING1B calibrated ChIP-seq (cChIPseq) datasets for control mESCs and an Scc1-AID auxin-inducible degron.

ABSTRACT: We examined 3D chromatin structure in the absence of cohesin (Scc1-AID auxin-inducible degron) and a control line (E14-Tir1) and found that PRC1 core promoter component RING1B was one of the most enriched proteins. Hence, we performed calibrated ChIP-seq experiments on the control (E14-Tir1) and the Scc1-AID mESC lines with a spike in of HEK293 human cells to further study this relationship.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Angelika Feldmann

PROVIDER: E-MTAB-7817 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells

Project description:The aim of the experiment was to gain a higher resolution for specific regions of interest to complement the Hi-C results. Capture-C experiments were performed on four-inducible degrons for Scc1, Ringb, Ring1b-Scc1 and CTCF, and Tir1 control, always in triplicates (three biological replicates per condition).

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DNA double-strand breaks and 3D chromatin conformation (Hi-C, 4C-seq, ChIP-seq)

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Project description:Polycomb group (PcG) proteins are required for normal differentiation and development, and their activity is found deregulated in cancer. PcG proteins are involved in gene silencing, however, whether they initiate or maintain transcriptional repression is a subject of debate. Here, we show that knockout of the Polycomb repressive complex 2 (PRC2) does not lead to significant gene expression changes in mouse embryonic stem cells (mESCs), and that it is dispensable for initiating silencing of target genes during differentiation. Transcriptional inhibition in mESCs is sufficient to induce genome-wide ectopic PRC2 recruitment to endogenous PcG target genes found in other tissues. PRC2 binding analysis shows that it is restricted to nucleosome-free CpG islands (CGIs) of un-transcribed genes. Our results show that it is the transcriptional state that governs PRC2 binding, and we propose that it binds by default to non-transcribed CGI genes to maintain their silenced state and to protect cell identity. RNA-seq time-course experiments during in vitro differentiation (0h, 24h, 48h and 72h) of Mus musculus wild-type E14 and Suz12 knock-out Embryonic Stem Cells with two biological replicates per condition.

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