Transcription Restart Establishes Chromatin Accessibility after DNA Replication

Research output: Contribution to journal › Journal article › Research › peer-review

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Transcription Restart Establishes Chromatin Accessibility after DNA Replication. / Stewart-Morgan, Kathleen R; Reverón-Gómez, Nazaret; Groth, Anja.

In: Molecular Cell, Vol. 75, No. 2, 2019, p. 284-297.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Stewart-Morgan, KR, Reverón-Gómez, N & Groth, A 2019, 'Transcription Restart Establishes Chromatin Accessibility after DNA Replication', Molecular Cell, vol. 75, no. 2, pp. 284-297. https://doi.org/10.1016/j.molcel.2019.04.033

APA

Stewart-Morgan, K. R., Reverón-Gómez, N., & Groth, A. (2019). Transcription Restart Establishes Chromatin Accessibility after DNA Replication. Molecular Cell, 75(2), 284-297. https://doi.org/10.1016/j.molcel.2019.04.033

Vancouver

Stewart-Morgan KR, Reverón-Gómez N, Groth A. Transcription Restart Establishes Chromatin Accessibility after DNA Replication. Molecular Cell. 2019;75(2):284-297. https://doi.org/10.1016/j.molcel.2019.04.033

Author

Stewart-Morgan, Kathleen R ; Reverón-Gómez, Nazaret ; Groth, Anja. / Transcription Restart Establishes Chromatin Accessibility after DNA Replication. In: Molecular Cell. 2019 ; Vol. 75, No. 2. pp. 284-297.

Bibtex

@article{67528bb13b74406d8093c6efc16fc597,
title = "Transcription Restart Establishes Chromatin Accessibility after DNA Replication",
abstract = "DNA replication is highly disruptive to chromatin, leading to eviction of nucleosomes, RNA polymerase, and regulatory factors. When and how transcription resumes on DNA following DNA replication is unknown. Here we develop a replication-coupled assay for transposase-accessible chromatin (repli-ATAC-seq) to investigate active chromatin restoration post-replication in mouse embryonic stem cells. We find that nascent chromatin is inaccessible and transcriptionally silenced, with accessibility and RNA polymerase occupancy re-appearing within 30 minutes. Chromatin accessibility restores differentially genome wide, with super enhancers regaining transcription factor occupancy faster than other genomic features. We also identify opportunistic and transiently accessible chromatin within gene bodies after replication. Systematic inhibition of transcription shows that transcription restart is required to re-establish active chromatin states genome wide and resolve opportunistic binding events resulting from DNA replication. Collectively, this establishes a central role for transcription in overcoming the genome-wide chromatin inaccessibility imposed by DNA replication every cell division.",
author = "Stewart-Morgan, {Kathleen R} and Nazaret Rever{\'o}n-G{\'o}mez and Anja Groth",
note = "Copyright {\textcopyright} 2019 Elsevier Inc. All rights reserved.",
year = "2019",
doi = "10.1016/j.molcel.2019.04.033",
language = "English",
volume = "75",
pages = "284--297",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - Transcription Restart Establishes Chromatin Accessibility after DNA Replication

AU - Stewart-Morgan, Kathleen R

AU - Reverón-Gómez, Nazaret

AU - Groth, Anja

N1 - Copyright © 2019 Elsevier Inc. All rights reserved.

PY - 2019

Y1 - 2019

N2 - DNA replication is highly disruptive to chromatin, leading to eviction of nucleosomes, RNA polymerase, and regulatory factors. When and how transcription resumes on DNA following DNA replication is unknown. Here we develop a replication-coupled assay for transposase-accessible chromatin (repli-ATAC-seq) to investigate active chromatin restoration post-replication in mouse embryonic stem cells. We find that nascent chromatin is inaccessible and transcriptionally silenced, with accessibility and RNA polymerase occupancy re-appearing within 30 minutes. Chromatin accessibility restores differentially genome wide, with super enhancers regaining transcription factor occupancy faster than other genomic features. We also identify opportunistic and transiently accessible chromatin within gene bodies after replication. Systematic inhibition of transcription shows that transcription restart is required to re-establish active chromatin states genome wide and resolve opportunistic binding events resulting from DNA replication. Collectively, this establishes a central role for transcription in overcoming the genome-wide chromatin inaccessibility imposed by DNA replication every cell division.

AB - DNA replication is highly disruptive to chromatin, leading to eviction of nucleosomes, RNA polymerase, and regulatory factors. When and how transcription resumes on DNA following DNA replication is unknown. Here we develop a replication-coupled assay for transposase-accessible chromatin (repli-ATAC-seq) to investigate active chromatin restoration post-replication in mouse embryonic stem cells. We find that nascent chromatin is inaccessible and transcriptionally silenced, with accessibility and RNA polymerase occupancy re-appearing within 30 minutes. Chromatin accessibility restores differentially genome wide, with super enhancers regaining transcription factor occupancy faster than other genomic features. We also identify opportunistic and transiently accessible chromatin within gene bodies after replication. Systematic inhibition of transcription shows that transcription restart is required to re-establish active chromatin states genome wide and resolve opportunistic binding events resulting from DNA replication. Collectively, this establishes a central role for transcription in overcoming the genome-wide chromatin inaccessibility imposed by DNA replication every cell division.

U2 - 10.1016/j.molcel.2019.04.033

DO - 10.1016/j.molcel.2019.04.033

M3 - Journal article

C2 - 31126739

VL - 75

SP - 284

EP - 297

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 2

ER -

ID: 225379684