Evidence map›Paper›PMID 22807480›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Chromatin-interaction compartment switch at developmentally regulated chromosomal domains reveals an unusual principle of chromatin folding.

Shin-ichiro Takebayashi, Vishnu Dileep, Tyrone Ryba, Jonathan H Dennis, David M Gilbert

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Mammalian DNA Replication Timing.Cold Spring Harbor perspectives in biology · 2021
    Review
  6. Review
  7. Article
  8. Transcription factors: building hubs in the 3D space.Cell cycle (Georgetown, Tex.) · 2020
    Review
  9. Control of DNA replication timing in the 3D genome.Nature reviews. Molecular cell biology · 2019
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

5 authors.

Shin-ichiro TakebayashiDepartment of Biological Science, Florida State University, Tallahassee, FL 32306, USA.
Vishnu Dileep
Tyrone Ryba
Jonathan H Dennis
David M Gilbert

Funding

UNDERSTANDING MECHANISMS OF hESC SELF-RENEWAL AND CELL FATE COMMITMENTP01GM085354 · NIGMS · UNIVERSITY OF GEORGIA · PI DALTON, STEPHEN · 2008 to 2018
$18.3M
NIGMS NIH HHS GM085354NIGMS NIH HHS P01 GM085354
6 · The paper itself

Abstract

Several 400- to 800-kb murine chromosome domains switch from early to late replication during loss of pluripotency, accompanied by a stable form of gene silencing that is resistant to reprogramming. We found that, whereas enhanced nuclease accessibility correlated with early replication genome-wide, domains that switch replication timing during differentiation were exceptionally inaccessible even when early-replicating. Nonetheless, two domains studied in detail exhibited substantial changes in transcriptional activity and higher-order chromatin unfolding confined to the region of replication timing change. Chromosome conformation capture (4C) data revealed that in the unfolded state in embryonic stem cells, these domains interacted preferentially with the early-replicating chromatin compartment, rarely interacting even with flanking late-replicating domains, whereas after differentiation, these same domains preferentially associated with late-replicating chromatin, including flanking domains. In both configurations they retained local boundaries of self-interaction, supporting the replication domain model of replication-timing regulation. Our results reveal a principle of developmentally regulated, large-scale chromosome folding involving a subnuclear compartment switch of inaccessible chromatin. This unusual level of regulation may underlie resistance to reprogramming in replication-timing switch regions.

Indexed as

AnimalsCell LineChromatinChromatin Assembly and DisassemblyChromosomes, MammalianDNA ReplicationEmbryonic Stem CellsGenome-Wide Association StudyMiceChromatin

Identifiers

PMID22807480
PMCPMC3411983

What OpenQuestion holds

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Registered trials

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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.