Evidence map›Paper›PMID 24013502›Full record

ArticleGenes & development2013

Epe1 recruits BET family bromodomain protein Bdf2 to establish heterochromatin boundaries.

Jiyong Wang, Xavier Tadeo, Haitong Hou, Patricia G Tu, James Thompson, John R Yates, Songtao Jia

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  5. Article
  6. A meiotic driver hijacks an epigenetic reader to disrupt mitosis in noncarrier offspring.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Clr4Nature communications · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Fission Yeast Mating-Type Switching Motto: "One-for-Two" and "Two-for-One".Microbiology and molecular biology reviews : MMBR · 2023
    Review
  14. Review
  15. Mechanisms of chromatin-based epigenetic inheritance.Science China. Life sciences · 2022
    Review
  16. Review
  17. Article
  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

7 authors at 2 institutions in 1 country.

Jiyong WangDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA;
Xavier Tadeo
Haitong Hou
Patricia G Tu
James Thompson
John R Yates
Songtao Jia
Columbia University · USScripps Research Institute · US

Funding

ZDS2P REGULATES SWE1P-DEPENDENT POLARIZED CELL GROWTH IN S CEREVISIAEP41RR011823 · NCRR · UNIVERSITY OF WASHINGTON · PI DAVIS, TRACY · 1996 to 2011
$24.7M
TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2012 to 2021
$20.7M
Mechanism of heterochromatin assemblyR01GM085145 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI JIA, SONGTAO · 2008 to 2017
$3.0M
NCRR NIH HHS P41 RR011823NCRR NIH HHS P41-RR011823NIGMS NIH HHS P41 GM103533NIGMS NIH HHS P41-GM103533NIGMS NIH HHS R01 GM085145NIGMS NIH HHS R01-GM085145
6 · The paper itself

Abstract

Heterochromatin spreading leads to the silencing of genes within its path, and boundary elements have evolved to constrain such spreading. In fission yeast, heterochromatin at centromeres I and III is flanked by inverted repeats termed IRCs, which are required for proper boundary functions. However, the mechanisms by which IRCs prevent heterochromatin spreading are unknown. Here, we identified Bdf2, which is homologous to the mammalian bromodomain and extraterminal (BET) family double bromodomain proteins involved in diverse types of cancers, as a factor required for proper boundary function at IRCs. Bdf2 is enriched at IRCs through its interaction with the boundary protein Epe1. The bromodomains of Bdf2 recognize acetylated histone H4 tails and antagonize Sir2-mediated deacetylation of histone H4K16. Furthermore, abolishing H4K16 acetylation (H4K16ac) with an H4K16R mutation promotes heterochromatin spreading, and mimicking H4K16ac by an H4K16Q mutation blocks heterochromatin spreading at IRCs. Our results thus illustrate a mechanism of establishing chromosome boundaries at specific sites through the recruitment of a factor that protects euchromatic histone modifications. They also reveal a previously unappreciated function of H4K16ac in cooperation with H3K9 methylation to regulate heterochromatin spreading.

Indexed as

Bromodomain Containing ProteinsGene SilencingHeterochromatinHistone AcetyltransferasesHistonesInsulator ElementsNuclear ProteinsProtein BindingProtein Structure, TertiarySchizosaccharomycesSchizosaccharomyces pombe ProteinsTranscription FactorsBDF2 protein, S pombeBromodomain Containing Proteinsepe1 protein, S pombeHeterochromatinHistone AcetyltransferasesHistonesNuclear ProteinsSchizosaccharomyces pombe Proteinssir2 protein, S pombeTranscription FactorsacetylationBETboundaryH4K16heterochromatin

Identifiers

PMID24013502
PMCPMC3778242
OpenAlexW2169934759

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.