Evidence map›Paper›PMID 25453095›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Direct interactions promote eviction of the Sir3 heterochromatin protein by the SWI/SNF chromatin remodeling enzyme.

Benjamin J Manning, Craig L Peterson

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. The Many Roles of BAF (mSWI/SNF) and PBAF Complexes in Cancer.Cold Spring Harbor perspectives in medicine · 2016
    Review
  11. Review
  12. Review
  13. 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

2 authors at 1 institution in 1 country.

Benjamin J ManningProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605.
Craig L PetersonProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605 craig.peterson@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Analysis of the yeast SWI1, SWI2, and SWI3 proteinsR37GM049650 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PETERSON, CRAIG L · 2006 to 2015
$4.9M
YEAST SWI1, SWI2, AND SWI3 PROTEINSR01GM049650 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PETERSON, CRAIG L · 1993 to 2016
$2.6M
NIGMS NIH HHS GM49650NIGMS NIH HHS R01 GM049650NIGMS NIH HHS R37 GM049650
6 · The paper itself

Abstract

Heterochromatin is a specialized chromatin structure that is central to eukaryotic transcriptional regulation and genome stability. Despite its globally repressive role, heterochromatin must also be dynamic, allowing for its repair and replication. In budding yeast, heterochromatin formation requires silent information regulators (Sirs) Sir2p, Sir3p, and Sir4p, and these Sir proteins create specialized chromatin structures at telomeres and silent mating-type loci. Previously, we found that the SWI/SNF chromatin remodeling enzyme can catalyze the ATP-dependent eviction of Sir3p from recombinant nucleosomal arrays, and this activity enhances early steps of recombinational repair in vitro. Here, we show that the ATPase subunit of SWI/SNF, Swi2p/Snf2p, interacts with the heterochromatin structural protein Sir3p. Two interaction surfaces are defined, including an interaction between the ATPase domain of Swi2p and the nucleosome binding, Bromo-Adjacent-Homology domain of Sir3p. A SWI/SNF complex harboring a Swi2p subunit that lacks this Sir3p interaction surface is unable to evict Sir3p from nucleosomes, even though its ATPase and remodeling activities are intact. In addition, we find that the interaction between Swi2p and Sir3p is key for SWI/SNF to promote resistance to replication stress in vivo and for establishment of heterochromatin at telomeres.

Indexed as

Models, MolecularAdenosine TriphosphatasesAnimalsBlotting, WesternChromatin Assembly and DisassemblyDNA PrimersElectrophoresis, Polyacrylamide GelEscherichia coliHeterochromatinHistonesNucleosomesOligonucleotidesPolymerase Chain ReactionRosaniline DyesSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeAdenosine TriphosphatasesCoomassie blueDNA PrimersHeterochromatinHistonesNucleosomesOligonucleotidesRosaniline DyesSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR3 protein, S cerevisiaeSNF2 protein, S cerevisiaeTranscription FactorsBAHchromatin remodelingheterochromatinSir3SWI/SNF

Identifiers

PMID25453095
PMCPMC4273332
OpenAlexW2017099128

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.