Evidence map›Paper›PMID 19638198›Full record

ArticleBMC molecular biology2009

Multiple histone modifications in euchromatin promote heterochromatin formation by redundant mechanisms in Saccharomyces cerevisiae.

Kitty F Verzijlbergen, Alex W Faber, Iris Je Stulemeijer, Fred van Leeuwen

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Ten principles of heterochromatin formation and function.Nature reviews. Molecular cell biology · 2018
    Review
  7. Spurious transcription factor binding: non-functional or genetically redundant?BioEssays : news and reviews in molecular, cellular and developmental biology · 2014
    Article
  8. Article
  9. Article
  10. Sirt1 suppresses RNA synthesis after UV irradiation in combined xeroderma pigmentosum group D/Cockayne syndrome (XP-D/CS) cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Chromatin structure following UV-induced DNA damage-repair or death?International journal of molecular sciences · 2011
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Kitty F VerzijlbergenFred van Leeuwen, Division of Gene Regulation B4, Netherlands Cancer Institute, The Netherlands. k.verzijlbergen@nki.nl
Alex W Faber
Iris Je Stulemeijer
Fred van Leeuwen
The Netherlands Cancer Institute · NLNetherlands Cancer Institute-Antoni van Leeuwenhoek Hospital · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMethylation of lysine 79 on histone H3 by Dot1 is required for maintenance of heterochromatin structure in yeast and humans. However, this histone modification occurs predominantly in euchromatin. Thus, Dot1 affects silencing by indirect mechanisms and does not act by the recruitment model commonly proposed for histone modifications. To better understand the role of H3K79 methylation gene silencing, we investigated the silencing function of Dot1 by genetic suppressor and enhancer analysis and examined the relationship between Dot1 and other global euchromatic histone modifiers.

resultWe determined that loss of H3K79 methylation results in a partial silencing defect that could be bypassed by conditions that promote targeting of Sir proteins to heterochromatin. Furthermore, the silencing defect in strains lacking Dot1 was dependent on methylation of H3K4 by Set1 and histone acetylation by Gcn5, Elp3, and Sas2 in euchromatin. Our study shows that multiple histone modifications associated with euchromatin positively modulate the function of heterochromatin by distinct mechanisms. Genetic interactions between Set1 and Set2 suggested that the H3K36 methyltransferase Set2, unlike most other euchromatic modifiers, negatively affects gene silencing.

conclusionOur genetic dissection of Dot1's role in silencing in budding yeast showed that heterochromatin formation is modulated by multiple euchromatic histone modifiers that act by non-overlapping mechanisms. We discuss how euchromatic histone modifiers can make negative as well as positive contributions to gene silencing by competing with heterochromatin proteins within heterochromatin, within euchromatin, and at the boundary between euchromatin and heterochromatin.

Indexed as

HeterochromatinGene DeletionGene Expression Regulation, FungalGene SilencingHistone AcetyltransferasesHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesNuclear ProteinsPhenotypeSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSirtuin 2SirtuinsDot1 protein, S cerevisiaeHeterochromatinHistone AcetyltransferasesHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesNuclear ProteinsSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSIR3 protein, S cerevisiaeSirtuin 2Sirtuins

Identifiers

PMID19638198
PMCPMC2724485
OpenAlexW2080551005

What OpenQuestion holds

Textmetadata
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.