Evidence map›Paper›PMID 34610305›Full record

ArticleCell reports2021

Collective regulation of chromatin modifications predicts replication timing during cell cycle.

Capucine Van Rechem, Fei Ji, Damayanti Chakraborty, Joshua C Black, Ruslan I Sadreyev, Johnathan R Whetstine

Abstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed.

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  8. Replication stress-induced nuclear hypertrophy alters chromatin topology and impacts cancer cell fitness.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Capucine Van RechemMassachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA; Department of Pathology, Stanford Medicine, Stanford, CA 94305, USA.
Fei JiDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Damayanti ChakrabortyMassachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA.
Joshua C BlackMassachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA.
Ruslan I SadreyevDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: sadreyev@molbio.mgh.harvard.edu.
Johnathan R WhetstineMassachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA; Cancer Signaling and Epigenetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Cancer Epigenetics Institute, Fox Chase Cancer Center, Philadelphia, PA 19111, USA. Electronic address: johnathan.whetstine@fccc.edu.

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Eric Andrew Ross · 1985 to 2026
$138.8M
ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Elizabeth Austen Lawson, Takara Leah Stanley · 1994 to 2026
$31.6M
Understanding the Role of Histone Demethylases and Heterochromatin in Cell CycleR01GM097360 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI WHETSTINE, JOHNATHAN R. · 2012 to 2020
$3.4M
NCI NIH HHS P30 CA006927NIDDK NIH HHS P30 DK040561NIGMS NIH HHS R01 GM097360
6 · The paper itself

Abstract

Replication timing (RT) associates with genome architecture, while having a mixed relationship to histone marks. By profiling replication at high resolution and assessing broad histone marks across the cell cycle at the resolution of RT with and without genetic perturbation, we address the causal relationship between histone marks and RT. Four primary chromatin states, including an uncharacterized H3K36me2 state, emerge and define 97% of the mappable genome. RT and local replication patterns (e.g., initiation zones) quantitatively associate with chromatin states, histone mark dynamics, and spatial chromatin structure. Manipulation of broad histone marks and enhancer elements by overexpressing the histone H3 lysine 9/36 tri-demethylase KDM4A impacts RT across 11% of the genome. Broad histone modification changes were strong predictors of the observed RT alterations. Lastly, replication within H3K36me2-enriched neighborhoods is sensitive to KDM4A overexpression and is controlled at a megabase scale. These studies establish a role for collective chromatin mark regulation in modulating RT.

Indexed as

Cell LineChromatinDNA Replication TimingEnhancer Elements, GeneticGenomeHistone CodeHumansJumonji Domain-Containing Histone DemethylasesMethylationS PhaseChromatinJumonji Domain-Containing Histone DemethylasesKDM4A protein, humanChIP-seqchromatin statesenhancersH3K27me3H3K36me2heterochromatinKDM4Alysine demethylasereplication timingRepli-seq

Identifiers

PMID34610305
PMCPMC8530517

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.