Evidence map›Paper›PMID 27340175›Full record

ArticleGenes & development2016

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

Chris C-S Hsiung, Caroline R Bartman, Peng Huang, Paul Ginart, Aaron J Stonestrom, Cheryl A Keller, Carolyne Face, Kristen S Jahn, Perry Evans, Laavanya Sankaranarayanan and 4 more

Abstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing 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

77 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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  6. Article
  7. The Kinetic Intron Hypothesis.bioRxiv : the preprint server for biology · 2026
    Article
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  11. Article
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  13. Review
  14. Review
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  20. Review

17 more citing papers are in PubMed but not listed here.

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

14 authors.

Chris C-S HsiungDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Caroline R BartmanDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Peng HuangDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;
Paul GinartPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA, Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Aaron J StonestromDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Cheryl A KellerDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Carolyne FaceDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;
Kristen S JahnDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;
Perry EvansDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;
Laavanya SankaranarayananDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA;
Belinda GiardineDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Ross C HardisonDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Arjun RajDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Gerd A BlobelDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008216 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI EPSTEIN, DOUGLAS J · 1987 to 2023
$8.3M
Regulation of Hemoglobin SwitchingR01HL119479 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI Gerd A Blobel · 2013 to 2026
$8.0M
HEMATOPOIESIS TRAINING GRANTT32DK007780 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI TONG, WEI · 1999 to 2023
$6.7M
Engineering and visualizing genome folding at high spatiotemporal resolutionU01HL129998 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BLOBEL, GERD A, PHILLIPS-CREMINS, JENNIFER ELIZABETH · 2015 to 2019
$4.2M
Epigenetic Control of Hematopoietic Gene ExpressionR37DK058044 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI BLOBEL, GERD A · 2010 to 2019
$3.7M
A Comprehensive Spatial Picture of Transcription in the NucleusDP2OD008514 · OD · UNIVERSITY OF PENNSYLVANIA · PI RAJ, ARJUN · 2011 to 2011
$2.4M
Validation and development of single nucleotide variant RNA FISH in single cells in culture and tissueR33EB019767 · NIBIB · UNIVERSITY OF PENNSYLVANIA · PI RAJ, ARJUN · 2014 to 2016
$1.1M
Global Predictions and Tests of Hematopoietic RegulationR56DK065806 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI BLOBEL, GERD A, BODINE, DAVID M. · 2014 to 2014
$224k
NHLBI NIH HHS R01 HL119479NHLBI NIH HHS U01 HL129998NIBIB NIH HHS R33 EB019767NIDDK NIH HHS R37 DK058044NIDDK NIH HHS R56 DK065806NIDDK NIH HHS T32 DK007780NIGMS NIH HHS T32 GM008216NIH HHS DP2 OD008514
6 · The paper itself

Abstract

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.

Indexed as

AnimalsCell CycleCell LineCells, CulturedChromatinDNA, IntergenicEnhancer Elements, GeneticErythroblastsG1 PhaseGenomeMiceMitosisPromoter Regions, GeneticTranscriptional ActivationUp-RegulationChromatinDNA, Intergenicchromatinepigeneticsmitosistranscription

Identifiers

PMID27340175
PMCPMC4926865

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.