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Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

ABSTRACT: Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

PROVIDER: PRJNA533460 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10002100_1.fastq.gz	Fastqsanger.gz
	SRR10002100_2.fastq.gz	Fastqsanger.gz
	SRR10002101_1.fastq.gz	Fastqsanger.gz
	SRR10002101_2.fastq.gz	Fastqsanger.gz
	SRR10002102_1.fastq.gz	Fastqsanger.gz

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Re-configuration of Chromatin Structure During the Mitosis-G1 Phase Progression

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Project description:During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. Here we exploited the M-phase to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to re-sculpting the genome in newborn nuclei. While CTCF appears to be dispensable for large scale post-mitotic compartmentalization, depletion of CTCF specifically during the M-phase to G1-phase transition alters the re-establishment of local short-range compartmentalization after mitosis. Without CTCF, structural loops fail to reform, leading to illegitimate contacts between cis-regulatory elements (CREs) and altered gene expression in G1-phase. Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF depleted cells. Boundary reformation is largely disrupted upon CTCF loss. Yet, a subset (~27%) of boundaries emerges normally in the absence of CTCF and is characterized by transitions in chromatin states. Reformation of gene domains can occur prior to the full onset of transcription and can be linked to tri-methylation at lysine 36 of histone 3 (H3K36me3), a mark stable throughout mitosis. The focus on the de novo formation of nuclear architecture during G1 entry yielded novel insights into how CTCF and the process of transcription contribute to the dynamic re-configuration of chromatin architecture during the mitosis to G1 phase progression.

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Project description:We report genome wide mapping of the histone variant H2A.Z during G0/G1 and mitosis in T24 bladder cancer cells. The results show that the broad enrichment pattern of H2A.Z near transcription start sites of active genes is maintained during mitosis. Furthermore, using H2A.Z localization to visualize nucleosome positioning near the start site, we see that the +1 nucleosome of active genes shifts upstream to occupy the transcription start sites during mitosis and the nucleosome depleted region is shortened. H2A.Z is also maintained on the -2 nucleosome which also shifts towrds the transcription start site during mitosis, further contributing to the shorteneing of the nucleosome depleted region. Examination of H2A.Z duing G0/G1 and mitosis in bladder cancer cells

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CTCF and transcription orchestrate chromatin structure re-configuration after mitosis

Project description:This SuperSeries is composed of the SubSeries listed below.

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CTCF and transcription influence chromatin structure re-configuration after mitosis.

Project description:During mitosis, transcription is globally attenuated and chromatin architecture is dramatically reconfigured. We exploited the M- to G1-phase progression to interrogate the contributions of the architectural factor CTCF and the process of transcription to genome re-sculpting in newborn nuclei. Depletion of CTCF during the M- to G1-phase transition alters short-range compartmentalization after mitosis. Chromatin domain boundary re-formation is impaired upon CTCF loss, but a subset of boundaries, characterized by transitions in chromatin states, is established normally. Without CTCF, structural loops fail to form, leading to illegitimate contacts between cis-regulatory elements (CREs). Transient CRE contacts that are normally resolved after telophase persist deeply into G1-phase in CTCF-depleted cells. CTCF loss-associated gains in transcription are often linked to increased, normally illegitimate enhancer-promoter contacts. In contrast, at genes whose expression declines upon CTCF loss, CTCF seems to function as a conventional transcription activator, independent of its architectural role. CTCF-anchored structural loops facilitate formation of CRE loops nested within them, especially those involving weak CREs. Transcription inhibition does not significantly affect global architecture or transcription start site-associated boundaries. However, ongoing transcription contributes considerably to the formation of gene domains, regions of enriched contacts along gene bodies. Notably, gene domains emerge in ana/telophase prior to completion of the first round of transcription, suggesting that epigenetic features in gene bodies contribute to genome reconfiguration prior to transcription. The focus on the de novo formation of nuclear architecture during G1 entry yields insights into the contributions of CTCF and transcription to chromatin architecture dynamics during the mitosis to G1-phase progression.

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