Evidence map›Paper›PMID 23771057›Full record

ArticleThe EMBO journal2013

Sir2 is required for Clr4 to initiate centromeric heterochromatin assembly in fission yeast.

Benjamin J Alper, Godwin Job, Rajesh K Yadav, Sreenath Shanker, Brandon R Lowe, Janet F Partridge

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
11.1field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Heterochromatin-based silencing of a foreign tandem repeat inbioRxiv : the preprint server for biology · 2025
    Article
  4. RiboCop surveils pre-rRNA processing by Dicer in cellular quiescence.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
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  7. Review
  8. Review
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Close to the edge: Heterochromatin at the nucleolar and nuclear peripheries.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Benjamin J AlperDepartment of Biochemistry, St Jude Children's Research Hospital, Memphis, TN 38105, USA.
Godwin Job
Rajesh K Yadav
Sreenath Shanker
Brandon R Lowe
Janet F Partridge
St. Jude Children's Research Hospital · USUniversity of Tennessee Health Science Center · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Establishment of HeterochromatinR01GM084045 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI PARTRIDGE, JANET F · 2008 to 2012
$1.8M
NCI NIH HHS P30 CA021765NCI NIH HHS P30 CA21765NIGMS NIH HHS R01 GM084045
6 · The paper itself

Abstract

Heterochromatin assembly in fission yeast depends on the Clr4 histone methyltransferase, which targets H3K9. We show that the histone deacetylase Sir2 is required for Clr4 activity at telomeres, but acts redundantly with Clr3 histone deacetylase to maintain centromeric heterochromatin. However, Sir2 is critical for Clr4 function during de novo centromeric heterochromatin assembly. We identified new targets of Sir2 and tested if their deacetylation is necessary for Clr4-mediated heterochromatin establishment. Sir2 preferentially deacetylates H4K16Ac and H3K4Ac, but mutation of these residues to mimic acetylation did not prevent Clr4-mediated heterochromatin establishment. Sir2 also deacetylates H3K9Ac and H3K14Ac. Strains bearing H3K9 or H3K14 mutations exhibit heterochromatin defects. H3K9 mutation blocks Clr4 function, but why H3K14 mutation impacts heterochromatin was not known. Here, we demonstrate that recruitment of Clr4 to centromeres is blocked by mutation of H3K14. We suggest that Sir2 deacetylates H3K14 to target Clr4 to centromeres. Further, we demonstrate that Sir2 is critical for de novo accumulation of H3K9me2 in RNAi-deficient cells. These analyses place Sir2 and H3K14 deacetylation upstream of Clr4 recruitment during heterochromatin assembly.

Indexed as

Cell Cycle ProteinsCentromereChromatin Assembly and DisassemblyHeterochromatinHistone-Lysine N-MethyltransferaseHistonesLysineMethyltransferasesMutationRNA InterferenceSchizosaccharomycesSchizosaccharomyces pombe ProteinsSubstrate SpecificityTelomereCell Cycle Proteinsclr4 protein, S pombeHeterochromatinHistone-Lysine N-MethyltransferaseHistonesLysineMethyltransferasesSchizosaccharomyces pombe Proteinssir2 protein, S pombe

Identifiers

PMID23771057
PMCPMC3770337
OpenAlexW2118489693

What OpenQuestion holds

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LicenceCC BY
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.