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A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE83293 | GEO | 2016/06/15

SECONDARY ACCESSION(S): PRJNA325495

REPOSITORIES: GEO

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A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition.

Project description:During mitosis, RNA polymerase II (Pol II) and many transcription factors dissociate from chromatin, and transcription ceases globally. Transcription is known to restart in bulk by telophase, but whether de novo transcription at the mitosis-G1 transition is in any way distinct from later in interphase remains unknown. We tracked Pol II occupancy genome-wide in mammalian cells progressing from mitosis through late G1. Unexpectedly, during the earliest rounds of transcription at the mitosis-G1 transition, ∼50% of active genes and distal enhancers exhibit a spike in transcription, exceeding levels observed later in G1 phase. Enhancer-promoter chromatin contacts are depleted during mitosis and restored rapidly upon G1 entry but do not spike. Of the chromatin-associated features examined, histone H3 Lys27 acetylation levels at individual loci in mitosis best predict the mitosis-G1 transcriptional spike. Single-molecule RNA imaging supports that the mitosis-G1 transcriptional spike can constitute the maximum transcriptional activity per DNA copy throughout the cell division cycle. The transcriptional spike occurs heterogeneously and propagates to cell-to-cell differences in mature mRNA expression. Our results raise the possibility that passage through the mitosis-G1 transition might predispose cells to diverge in gene expression states.

| S-EPMC4926865 | biostudies-literature

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-15 | E-GEOD-83293 | biostudies-arrayexpress

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Hist]

Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous). Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.

2016-06-15 | E-GEOD-83255 | biostudies-arrayexpress

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Pol2ChIP]

Project description:ChIP-seq of total Pol II in G1E ER4 cell line at time points after mitosis. Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.

2016-06-15 | E-GEOD-83263 | biostudies-arrayexpress

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Pol2ChIP]

Project description:ChIP-seq of total Pol II in G1E ER4 cell line at time points after mitosis.

2016-06-15 | GSE83263 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Hist]

Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous).

2016-06-15 | GSE83255 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [CaptureC]

Project description:Capture-C of G1E ER4 cell line in a nocodazole arrest-release experiment anchored at multiple gene promoters to quantify long-range chromatin interactions at the mitosis-G1 transition.

2016-06-15 | GSE83290 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition

Project description:A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition

| PRJNA325495 | ENA

Hierarchical reactivation of transcription during mitosis-to-G1 transition by Brn2 and Ascl1 in neural stem cells.

Project description:During mitosis, chromatin condensation is accompanied by a global arrest of transcription. Recent studies suggest transcriptional reactivation upon mitotic exit occurs in temporally coordinated waves, but the underlying regulatory principles have yet to be elucidated. In particular, the contribution of sequence-specific transcription factors (TFs) remains poorly understood. Here we report that Brn2, an important regulator of neural stem cell identity, associates with condensed chromatin throughout cell division, as assessed by live-cell imaging of proliferating neural stem cells. In contrast, the neuronal fate determinant Ascl1 dissociates from mitotic chromosomes. ChIP-seq analysis reveals that Brn2 mitotic chromosome binding does not result in sequence-specific interactions prior to mitotic exit, relying mostly on electrostatic forces. Nevertheless, surveying active transcription using single-molecule RNA-FISH against immature transcripts reveals differential reactivation kinetics for key targets of Brn2 and Ascl1, with transcription onset detected in early (anaphase) versus late (early G1) phases, respectively. Moreover, by using a mitotic-specific dominant-negative approach, we show that competing with Brn2 binding during mitotic exit reduces the transcription of its target gene Nestin Our study shows an important role for differential binding of TFs to mitotic chromosomes, governed by their electrostatic properties, in defining the temporal order of transcriptional reactivation during mitosis-to-G1 transition.

| S-EPMC8247608 | biostudies-literature

Chromatin structure dynamics during the mitosis-to-G1 phase transition.

Project description:Features of higher-order chromatin organization-such as A/B compartments, topologically associating domains and chromatin loops-are temporarily disrupted during mitosis1,2. Because these structures are thought to influence gene regulation, it is important to understand how they are re-established after mitosis. Here we examine the dynamics of chromosome reorganization by Hi-C after mitosis in highly purified, synchronous mouse erythroid cell populations. We observed rapid establishment of A/B compartments, followed by their gradual intensification and expansion. Contact domains form from the 'bottom up'-smaller subTADs are formed initially, followed by convergence into multi-domain TAD structures. CTCF is partially retained on mitotic chromosomes and immediately resumes full binding in ana/telophase. By contrast, cohesin is completely evicted from mitotic chromosomes and regains focal binding at a slower rate. The formation of CTCF/cohesin co-anchored structural loops follows the kinetics of cohesin positioning. Stripe-shaped contact patterns-anchored by CTCF-grow in length, which is consistent with a loop-extrusion process after mitosis. Interactions between cis-regulatory elements can form rapidly, with rates exceeding those of CTCF/cohesin-anchored contacts. Notably, we identified a group of rapidly emerging transient contacts between cis-regulatory elements in ana/telophase that are dissolved upon G1 entry, co-incident with the establishment of inner boundaries or nearby interfering chromatin loops. We also describe the relationship between transcription reactivation and architectural features. Our findings indicate that distinct but mutually influential forces drive post-mitotic chromatin reconfiguration.

| S-EPMC6895436 | biostudies-literature

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