Evidence map›Paper›PMID 27920256›Full record

ArticleMolecular and cellular biology2017

A Transcription Factor Pulse Can Prime Chromatin for Heritable Transcriptional Memory.

Aimee Iberg-Badeaux, Samuel Collombet, Benoit Laurent, Chris van Oevelen, Kuo-Kai Chin, Denis Thieffry, Thomas Graf, Yang Shi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact, top 90% of its field
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

10 citing papers in PubMed, 17 citations in OpenAlex.

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  10. NScience advances · 2021
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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

8 authors at 4 institutions in 3 countries.

Aimee Iberg-BadeauxDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA.
Samuel CollombetComputational Systems Biology Team, Institut de Biologie de l'Ecole Normale Supérieure, CNRS UMR8197, INSERM U1024, Ecole Normale Supérieure, PSL Research University, Paris, France.
Benoit LaurentDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA.
Chris van OevelenCenter for Genomic Regulation, Barcelona, Spain.
Kuo-Kai ChinDepartment of Newborn Medicine, Boston Children's Hospital, Boston, Massachusetts, USA.
Denis ThieffryComputational Systems Biology Team, Institut de Biologie de l'Ecole Normale Supérieure, CNRS UMR8197, INSERM U1024, Ecole Normale Supérieure, PSL Research University, Paris, France.
Thomas GrafCenter for Genomic Regulation, Barcelona, Spain Thomas.Graf@crg.eu yang_shi@hms.harvard.edu.
Yang ShiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA Thomas.Graf@crg.eu yang_shi@hms.harvard.edu.
Boston Children's Hospital · USCentre for Genomic Regulation · ESInserm · FRUniversité Paris Sciences et Lettres · FR

Funding

Novel epigenetic mechanisms in neuronal development and cognitive functionR01MH096066 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI ARLOTTA, PAOLA, POMEROY, SCOTT LOREN · 2012 to 2022
$6.1M
NIMH NIH HHS R01 MH096066
6 · The paper itself

Abstract

Short-term and long-term transcriptional memory is the phenomenon whereby the kinetics or magnitude of gene induction is enhanced following a prior induction period. Short-term memory persists within one cell generation or in postmitotic cells, while long-term memory can survive multiple rounds of cell division. We have developed a tissue culture model to study the epigenetic basis for long-term transcriptional memory (LTTM) and subsequently used this model to better understand the epigenetic mechanisms that enable heritable memory of temporary stimuli. We find that a pulse of transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) induces LTTM on a subset of target genes that survives nine cell divisions. The chromatin landscape at genes that acquire LTTM is more repressed than at those genes that do not exhibit memory, akin to a latent state. We show through chromatin immunoprecipitation (ChIP) and chemical inhibitor studies that RNA polymerase II (Pol II) elongation is important for establishing memory in this model but that Pol II itself is not retained as part of the memory mechanism. More generally, our work reveals that a transcription factor involved in lineage specification can induce LTTM and that failure to rerepress chromatin is one epigenetic mechanism underlying transcriptional memory.

Indexed as

Transcription, GeneticCCAAT-Enhancer-Binding Protein-alphaChromatinEnhancer Elements, GeneticGene Expression RegulationHistonesLipopolysaccharidesLysineMethylationProtein BindingRNA Polymerase IITranscription FactorsCCAAT-Enhancer-Binding Protein-alphaChromatinHistonesLipopolysaccharidesLysineRNA Polymerase IITranscription Factorschromatinepigeneticinflammationprimingtrained immunitytranscriptional memory

Identifiers

PMID27920256
PMCPMC5288571
OpenAlexW2560392633

What OpenQuestion holds

Textmetadata
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.