Evidence map›Paper›PMID 20950625›Full record

ArticleJournal of molecular biology2010

Reversal of a mutator activity by a nearby fidelity-neutral substitution in the RB69 DNA polymerase binding pocket.

Anna Trzemecka, Agata Jacewicz, Geraldine T Carver, John W Drake, Anna Bebenek

Abstract read
In one paragraph

Article in Journal of molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Antimutator variants of DNA polymerases.Critical reviews in biochemistry and molecular biology · 2011
    Review
  7. Article
  8. Genome studies at the PAG 2011 conference.Functional & integrative genomics · 2011
    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 2 institutions in 2 countries.

Anna TrzemeckaDepartment of Molecular Biology, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawinskiego 5a, 02-104 Warsaw, Poland.
Agata Jacewicz
Geraldine T Carver
John W Drake
Anna Bebenek
Institute of Biochemistry and Biophysics, Polish Academy of Sciences · PLNational Institute of Environmental Health Sciences · US

Funding

STRUCTURAL BASIS OF POLYMERASE FIDELITYZ01ES061054 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI DRAKE, JOHN W. · 1998 to 2008
$166k
Structural Basis of Polymerase FidelityZIAES061054 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI DRAKE, JOHN W. · 2009 to 2011
$45k
Intramural NIH HHS Z01 ES061054
6 · The paper itself

Abstract

Phage RB69 B-family DNA polymerase is responsible for the overall high fidelity of RB69 DNA synthesis. Fidelity is compromised when conserved Tyr567, one of the residues that form the nascent polymerase base-pair binding pocket, is replaced by alanine. The Y567A mutator mutant has an enlarged binding pocket and can incorporate and extend mispairs efficiently. Ser565 is a nearby conserved residue that also contributes to the binding pocket, but a S565G replacement has only a small impact on DNA replication fidelity. When Y567A and S565G replacements were combined, mutator activity was strongly decreased compared to that with Y567A replacement alone. Analyses conducted both in vivo and in vitro revealed that, compared to Y567A replacement alone, the double mutant mainly reduced base substitution mutations and, to a lesser extent, frameshift mutations. The decrease in mutation rates was not due to increased exonuclease activity. Based on measurements of DNA binding affinity, mismatch insertion, and mismatch extension, we propose that the recovered fidelity of the double mutant may result, in part, from an increased dissociation of the enzyme from DNA, followed by the binding of the same or another polymerase molecule in either exonuclease mode or polymerase mode. An additional antimutagenic factor may be a structural alteration in the polymerase binding pocket described in this article.

Indexed as

Mutation, MissenseAmino Acid SubstitutionBase SequenceBinding SitesDNA-Directed DNA PolymeraseDNA, ViralFrameshift MutationKineticsModels, MolecularMolecular Sequence DataMutant ProteinsMyoviridaePoint MutationProtein BindingProtein Structure, TertiaryViral Proteinsbacteriophage RB69 DNA polymeraseDNA-Directed DNA PolymeraseDNA, ViralMutant ProteinsViral Proteins

Identifiers

PMID20950625
PMCPMC2991499
OpenAlexW2038824912

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.