Evidence map›Paper›PMID 15314145›Full record

ArticleMolecular and cellular biology2004

Saccharomyces cerevisiae Srs2 DNA helicase selectively blocks expansions of trinucleotide repeats.

Saumitri Bhattacharyya, Robert S Lahue

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. 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
2.9field-weighted citation impact, top 9% 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, 80 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Meiosis-specific recombinase Dmc1 is a potent inhibitor of the Srs2 antirecombinase.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Review
  7. Article
  8. Review
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  10. Article
  11. Review
  12. Break-induced replication: an unhealthy choice for stress relief?Nature structural & molecular biology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The balancing act of DNA repeat expansions.Current opinion in genetics & development · 2013
    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

2 authors at 1 institution in 1 country.

Saumitri BhattacharyyaEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Box 986805, Omaha, NE 68198-6805, USA.
Robert S Lahue
University of Nebraska Medical Center · US

Funding

TRIPLET REPEAT INSTABILITY IN YEAST AND HUMAN CELLSR01GM061961 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BESSHO, TADAYOSHI · 2000 to 2007
$2.1M
NCI NIH HHS T32 CA09746NIGMS NIH HHS GM61961NIGMS NIH HHS R01 GM061961
6 · The paper itself

Abstract

Trinucleotide repeats (TNRs) undergo frequent mutations in families afflicted with certain neurodegenerative disorders and in model organisms. TNR instability is modulated both by the repeat tract itself and by cellular proteins. Here we identified the Saccharomyces cerevisiae DNA helicase Srs2 as a potent and selective inhibitor of expansions. srs2 mutants had up to 40-fold increased expansion rates of CTG, CAG, and CGG repeats. The expansion phenotype was specific, as mutation rates at dinucleotide repeats, at unique sequences, or for TNR contractions in srs2 mutants were not altered. Srs2 is known to suppress inappropriate genetic recombination; however, the TNR expansion phenotype of srs2 mutants was largely independent of RAD51 and RAD52. Instead, Srs2 mainly functioned with DNA polymerase delta to block expansions. The helicase activity of Srs2 was important, because a point mutant lacking ATPase function was defective in blocking expansions. Purified Srs2 was substantially better than bacterial UvrD helicase at in vitro unwinding of a DNA substrate that mimicked a TNR hairpin. Disruption of the related helicase gene SGS1 did not lead to excess expansions, nor did wild-type SGS1 suppress the expansion phenotype of an srs2 strain. We conclude that Srs2 selectively blocks triplet repeat expansions through its helicase activity and primarily in conjunction with polymerase delta.

Indexed as

Trinucleotide Repeat ExpansionTrinucleotide RepeatsDNA HelicasesDNA Polymerase IIIGenomic InstabilityMutationNucleic Acid ConformationPhenotypeRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA HelicasesDNA Polymerase IIISaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiae

Identifiers

PMID15314145
PMCPMC507003
OpenAlexW2059737494

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.