Evidence map›Paper›PMID 19126674›Full record

ArticleJournal of cell science2009

Combinatorial probabilistic chromatin interactions produce transcriptional heterogeneity.

Ty C Voss, R Louis Schiltz, Myong-Hee Sung, Thomas A Johnson, Sam John, Gordon L Hager

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Reduction in gene expression noise by targeted increase in accessibility at gene loci.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  13. Article
  14. Complex dynamics of transcription regulation.Biochimica et biophysica acta · 2012
    Review
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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 at 2 institutions in 1 country.

Ty C VossLaboratory of Receptor Biology and Gene Expression, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
R Louis Schiltz
Myong-Hee Sung
Thomas A Johnson
Sam John
Gordon L Hager
Center for Cancer Research · USNational Cancer Institute · US

Funding

Chromatin Structure and Gene ExpressionZIABC005450 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON L · 2009 to 2025
$35.2M
Function of Steroid Receptors in Subcellular CompartmentsZIABC010027 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON L · 2009 to 2025
$8.7M
FUNCTION OF STEROID RECEPTORS IN SUBCELLULAR COMPARTMENTSZ01BC010027 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON · 1996 to 2008
$492k
Intramural NIH HHS
6 · The paper itself

Abstract

Gene regulation often appears deterministic in the average cell population, but transcription is a probabilistic process at the single-cell level. Although many mechanisms are invoked to account for this behavior, it is difficult to determine how cell-to-cell variation in the interactions of transcription factors with target chromatin impact transcriptional output. Here, we use cells that contain a 200-copy tandem array of promoter or reporter gene units to simultaneously visualize transient interaction, equilibrium or steady-state binding of fluorescent-protein-labeled glucocorticoid receptor with its DNA response elements, the recruitment of diverse coregulators, and transcriptional output at the single-cell level. These regulatory proteins associate with target chromatin via a probabilistic mechanism that produces cell-to-cell variability in binding. The multiple steps of this process are partially independent and differ between individual regulators. The association level of each regulator influences the transcriptional output in individual cells, but this does not account for all transcriptional heterogeneity. Additionally, specific combinatorial interactions of the glucocorticoid receptor and coregulators with response elements regulate transcription at the single-cell level. Like many endogenous genes, the average array transcriptional activity evolves over time. This apparently deterministic average temporal promoter progression involves changes in the probability that specific combinatorial glucocorticoid receptor and coregulator interactions will occur on the response elements in single cells. These data support the emerging ;return-to-template' transcription model, which mechanistically unifies the observed extremely transient interactions between the transcription factor and response elements, cell-to-cell variability in steady-state association of factors with chromatin, and the resulting heterogeneous gene expression between individual cells.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsCell Line, TumorChromatinGenes, ReporterMammary Tumor Virus, MouseMicePromoter Regions, GeneticReceptors, GlucocorticoidTranscriptional ActivationTranscription FactorsChromatinReceptors, GlucocorticoidTranscription Factors

Identifiers

PMID19126674
PMCPMC2724732
OpenAlexW1973277418

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.