Evidence map›Paper›PMID 19782027›Full record

ArticleMolecular cell2009

Reconstitution of heterochromatin-dependent transcriptional gene silencing.

Aaron Johnson, Geng Li, Timothy W Sikorski, Stephen Buratowski, Christopher L Woodcock, Danesh Moazed

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
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  4. Two-way feedback between chromatin compaction and histone modification state explainsProceedings of the National Academy of Sciences of the United States of America · 2024
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  17. SIR proteins create compact heterochromatin fibers.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  18. Article
  19. Review
  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

6 authors at 3 institutions in 1 country.

Aaron JohnsonDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Geng Li
Timothy W Sikorski
Stephen Buratowski
Christopher L Woodcock
Danesh Moazed
Harvard University · USHoward Hughes Medical Institute · USUniversity of Massachusetts Amherst · US

Funding

The RNA polymerase II transcription complexR01GM046498 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BURATOWSKI, STEPHEN · 1996 to 2024
$9.4M
MECHANISM OF ACTION OF YEAST SILENCING COMPLEXESR01GM061641 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI MOAZED, DANESH · 2000 to 2014
$3.9M
Mechanistic Studies of silent chromatin spreadingF32GM078799 · NIGMS · HARVARD MEDICAL SCHOOL · PI JOHNSON, AARON M. · 2006 to 2008
$139k
RNA POLYMERASE II TRANSCRIPTION INITIATION COMPLEXR29GM046498 · NIGMS · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI BURATOWSKI, STEPHEN · 1991 to 1995
–
Howard Hughes Medical InstituteNIGMS NIH HHS F32 GM078799NIGMS NIH HHS GM061641NIGMS NIH HHS GM46498NIGMS NIH HHS R01 GM046498NIGMS NIH HHS R01 GM061641
6 · The paper itself

Abstract

Heterochromatin assembly in budding yeast requires the SIR complex, which contains the NAD-dependent deacetylase Sir2 and the Sir3 and Sir4 proteins. Sir3 binds to nucleosomes containing deacetylated histone H4 lysine 16 (H4K16) and, with Sir4, promotes spreading of Sir2 and deacetylation along the chromatin fiber. Combined action of histone modifying and binding activities is a conserved hallmark of heterochromatin, but the relative contribution of each activity to silencing has remained unclear. Here, we reconstitute SIR-chromatin complexes using purified components and show that the SIR complex efficiently deacetylates chromatin templates and promotes the assembly of altered structures that silence Gal4-VP16-activated transcription. Silencing requires all three Sir proteins, even with fully deacetylated chromatin, and involves the specific association of Sir3 with deacetylated H4K16. These results define a minimal set of components that mediate heterochromatic gene silencing and demonstrate distinct contributions for histone deacetylation and nucleosome binding in the silencing mechanism.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, FungalGene SilencingTranscription, GeneticAcetylationAdenosine TriphosphatasesCell Cycle ProteinsDNA-Binding ProteinsDNA Restriction EnzymesHeterochromatinHistone DeacetylasesHistonesLysineMultiprotein ComplexesMutationNADAdenosine TriphosphatasesCell Cycle ProteinsDNA-Binding ProteinsDNA Restriction EnzymesHeterochromatinHistone DeacetylasesHistonesISW1 protein, S cerevisiaeLysineMultiprotein ComplexesNADNAP1 protein, S cerevisiaeNuclear ProteinsNucleosome Assembly Protein 1RNA Polymerase IIRNA Polymerase IIISaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSIR3 protein, S cerevisiaeSIR4 protein, S cerevisiaeSirtuin 2Sirtuins

Identifiers

PMID19782027
PMCPMC2842978
OpenAlexW2045090702

What OpenQuestion holds

Textmetadata
LicenceTDM
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.