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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE83290 | GEO | 2016/06/15

SECONDARY ACCESSION(S): PRJNA325492

REPOSITORIES: GEO

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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 [Hist]

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2016-06-15 | GSE83255 | GEO

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]

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2016-06-15 | GSE83263 | GEO

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.

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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

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

2016-06-15 | GSE83293 | 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

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Genome-wide map of transcription factor GATA1 occupancy during mitosis in G1E ER4+E2 cells

Project description:Tissue-specific transcription patterns are preserved throughout cell divisions to maintain lineage fidelity. We investigated whether transcription factor GATA1 plays a role in transmitting hematopoietic gene expression programs through mitosis when transcription is transiently silenced. Live cell imaging revealed that a fraction of GATA1 is retained focally within mitotic chromatin. ChIP-seq of highly purified mitotic cells uncovered that key hematopoietic regulatory genes are occupied by GATA1 in mitosis. The GATA1 co- regulators FOG1 and TAL1 dissociate from mitotic chromatin, suggesting that GATA1 functions as platform for their postmitotic recruitment. Mitotic GATA1 target genes tend to re-activate more rapidly upon entry into G1 than genes from which GATA1 dissociates. A novel system designed to destroy GATA1 specifically during mitosis revealed that mitotic occupancy is required for rapid target gene reactivation. These studies suggest a requirement of mitotic “bookmarking” by GATA1 for the faithful propagation of cell type-specific transcription programs through cell division GATA1 occupancy profiles in mitotic G1E-ER4 +E2 cells generated by ChIP-sequencing. ChIP input DNA was sequenced as control. Previously reported (GSE18164) GATA1 occupancy in asynchrnous G1E-ER4 +E2 cells was analysed and compared with mitotic GATA1 occupancy.

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