Evidence map›Paper›PMID 24896181›Full record

ArticleNature2014

Avoidance of ribonucleotide-induced mutations by RNase H2 and Srs2-Exo1 mechanisms.

Catherine J Potenski, Hengyao Niu, Patrick Sung, Hannah L Klein

Open access · greenAbstract read
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Review
  7. Specific Human ATR and ATM Inhibitors Modulate Single Strand DNA Formation inFrontiers in cellular and infection microbiology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. DNA duplex recognition activates Exo1 nuclease activity.The Journal of biological chemistry · 2019
    Article
  16. Resolution of a complex crisis at DNA 3' termini.Nature structural & molecular biology · 2019
    Article
  17. Review
  18. Article
  19. 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
  20. Article

1 more citing papers are in PubMed but not listed here.

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.

Catherine J Potenski1] Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA [2].
Hengyao Niu1] Molecular Biophysics and Biochemistry, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA [2].
Patrick SungMolecular Biophysics and Biochemistry, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA.
Hannah L KleinDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
New York University · USYale University · US

Funding

Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
YEAST DNA REPAIR GENES AND PROTEINS OF THE RAD52 GROUPR01ES007061 · NIEHS · YALE UNIVERSITY · PI Patrick Sung · 1995 to 2026
$9.4M
DNA HELICASES IN RECOMBINATION AND REPAIRR01GM053738 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KLEIN, HANNAH L. · 1997 to 2010
$2.4M
Mechanisms and Crosstalk of DNA Break Resection PathwaysK99ES021441 · NIEHS · YALE UNIVERSITY · PI NIU, HENGYAO · 2012 to 2013
$180k
NCATS NIH HHS UL1 TR000142NIEHS NIH HHS K99 ES021441NIEHS NIH HHS K99ES021441NIEHS NIH HHS R01 ES007061NIEHS NIH HHS R01ES007061NIGMS NIH HHS R01 GM053738NIGMS NIH HHS R01GM053738
6 · The paper itself

Abstract

Srs2 helicase is known to dismantle nucleofilaments of Rad51 recombinase to prevent spurious recombination events and unwind trinucleotide sequences that are prone to hairpin formation. Here we document a new, unexpected genome maintenance role of Srs2 in the suppression of mutations arising from mis-insertion of ribonucleoside monophosphates during DNA replication. In cells lacking RNase H2, Srs2 unwinds DNA from the 5' side of a nick generated by DNA topoisomerase I at a ribonucleoside monophosphate residue. In addition, Srs2 interacts with and enhances the activity of the nuclease Exo1, to generate a DNA gap in preparation for repair. Srs2-Exo1 thus functions in a new pathway of nick processing-gap filling that mediates tolerance of ribonucleoside monophosphates in the genome. Our results have implications for understanding the basis of Aicardi-Goutières syndrome, which stems from inactivation of the human RNase H2 complex.

Indexed as

AnimalsCell LineDNA DamageDNA HelicasesEscherichia coliExodeoxyribonucleasesGenomic InstabilityMutationRibonuclease HRibonucleotidesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA Helicasesexodeoxyribonuclease IExodeoxyribonucleasesRibonuclease Hribonuclease HIIRibonucleotidesSaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiae

Identifiers

PMID24896181
PMCPMC4140095
OpenAlexW2031205269

What OpenQuestion holds

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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.