Evidence map›Paper›PMID 23150573›Full record

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

Nucleosome-depleted chromatin gaps recruit assembly factors for the H3.3 histone variant.

Jonathan I Schneiderman, Guillermo A Orsi, Kelly T Hughes, Benjamin Loppin, Kami Ahmad

Open access · bronzeAbstract 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 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025
    Review
  4. Article
  5. Article
  6. Remodeling of perturbed chromatin can initiate de novo transcriptional and post-transcriptional silencing.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Review
  8. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Cell Fate Decisions in the Wake of Histone H3 Deposition.Frontiers in cell and developmental biology · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

1 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

5 authors at 3 institutions in 2 countries.

Jonathan I SchneidermanDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA.
Guillermo A Orsi
Kelly T Hughes
Benjamin Loppin
Kami Ahmad
Harvard University · USCentre National de la Recherche Scientifique · FRMemorial Sloan Kettering Cancer Center · US

Funding

Genomic Functions of Nucleosome DynamicsR01GM098349 · NIGMS · HARVARD MEDICAL SCHOOL · PI AHMAD, KAMRAN · 2013 to 2016
$1.3M
NIGMS NIH HHS R01 GM098349
6 · The paper itself

Abstract

Most nucleosomes that package eukaryotic DNA are assembled during DNA replication, but chromatin structure is routinely disrupted in active regions of the genome. Replication-independent nucleosome replacement using the H3.3 histone variant efficiently repackages these regions, but how histones are recruited to these sites is unknown. Here, we use an inducible system that produces nucleosome-depleted chromatin at the Hsp70 genes in Drosophila to define steps in the mechanism of nucleosome replacement. We find that the Xnp chromatin remodeler and the Hira histone chaperone independently bind nucleosome-depleted chromatin. Surprisingly, these two factors are only displaced when new nucleosomes are assembled. H3.3 deposition assays reveal that Xnp and Hira are required for efficient nucleosome replacement, and double-mutants are lethal. We propose that Xnp and Hira recognize exposed DNA and serve as a binding platform for the efficient recruitment of H3.3 predeposition complexes to chromatin gaps. These results uncover the mechanisms by which eukaryotic cells actively prevent the exposure of DNA in the nucleus.

Indexed as

AnimalsChromatinChromatin ImmunoprecipitationDrosophilaHistonesHSP70 Heat-Shock ProteinsNucleosomesChromatinHistonesHSP70 Heat-Shock ProteinsNucleosomes

Identifiers

PMID23150573
PMCPMC3511725
OpenAlexW2167099695

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.