Evidence map›Paper›PMID 19766565›Full record

ArticleCell2009

Recombinational repair within heterochromatin requires ATP-dependent chromatin remodeling.

Manisha Sinha, Shinya Watanabe, Aaron Johnson, Danesh Moazed, Craig L Peterson

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. SIR proteins create compact heterochromatin fibers.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Review
  11. Article
  12. Review
  13. DNA repair goes hip-hop: SMARCA and CHD chromatin remodellers join the break dance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  14. And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  15. The INO80 remodeller in transcription, replication and repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 3 institutions in 1 country.

Manisha SinhaUniversity of Massachusetts Medical School, Worcester, MA 01605, USA.
Shinya Watanabe
Aaron Johnson
Danesh Moazed
Craig L Peterson
University of Massachusetts Chan Medical School · USHarvard University · USHoward Hughes Medical Institute · US

Funding

YEAST CHROMATIN STRUCTURE/FUNCTIONR01GM054096 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PETERSON, CRAIG L · 1997 to 2017
$5.7M
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
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
Howard Hughes Medical InstituteNIGMS NIH HHS F32 GM078799NIGMS NIH HHS GM061641NIGMS NIH HHS GM54096NIGMS NIH HHS R01 GM054096NIGMS NIH HHS R01 GM061641NIGMS NIH HHS R37 GM049650
6 · The paper itself

Abstract

Heterochromatin plays a key role in protection of chromosome integrity by suppressing homologous recombination. In Saccharomyces cerevisiae, Sir2p, Sir3p, and Sir4p are structural components of heterochromatin found at telomeres and the silent mating-type loci. Here we have investigated whether incorporation of Sir proteins into minichromosomes regulates early steps of recombinational repair in vitro. We find that addition of Sir3p to a nucleosomal substrate is sufficient to eliminate yRad51p-catalyzed formation of joints, and that this repression is enhanced by Sir2p/Sir4p. Importantly, Sir-mediated repression requires histone residues that are critical for silencing in vivo. Moreover, we demonstrate that the SWI/SNF chromatin-remodeling enzyme facilitates joint formation by evicting Sir3p, thereby promoting subsequent Rad54p-dependent formation of a strand invasion product. These results suggest that recombinational repair in the context of heterochromatin presents additional constraints that can be overcome by ATP-dependent chromatin-remodeling enzymes.

Indexed as

Chromatin Assembly and DisassemblyDNA RepairRecombination, GeneticAdenosine TriphosphateChromosomal Proteins, Non-HistoneHeterochromatinHistone DeacetylasesSaccharomyces cerevisiaeSilent Information Regulator Proteins, Saccharomyces cerevisiaeSirtuin 2SirtuinsTranscription FactorsAdenosine TriphosphateChromosomal Proteins, Non-HistoneHeterochromatinHistone DeacetylasesSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSIR3 protein, S cerevisiaeSIR4 protein, S cerevisiaeSirtuin 2SirtuinsSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID19766565
PMCPMC2791047
OpenAlexW2044904363

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.