Evidence map›Paper›PMID 32644157›Full record

ArticleNucleic acids research2020

Resolving Toxic DNA repair intermediates in every E. coli replication cycle: critical roles for RecG, Uup and RadD.

Zachary J Romero, Stefanie H Chen, Thomas Armstrong, Elizabeth A Wood, Antoine van Oijen, Andrew Robinson, Michael M Cox

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Identification ofJournal of bacteriology · 2023
    Article
  6. Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023
    Review
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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

7 authors at 3 institutions in 2 countries.

Zachary J RomeroDepartment of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.
Stefanie H ChenBiotechnology Program, North Carolina State University, Raleigh, NC 27695, USA.
Thomas ArmstrongMolecular Horizons Institute and School of Chemistry, University of Wollongong, Wollongong, Australia.
Elizabeth A WoodDepartment of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.
Antoine van OijenMolecular Horizons Institute and School of Chemistry, University of Wollongong, Wollongong, Australia.
Andrew RobinsonMolecular Horizons Institute and School of Chemistry, University of Wollongong, Wollongong, Australia.
Michael M CoxDepartment of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.
University of Wisconsin–Madison · USUniversity of Wollongong · AUNorth Carolina State University · US

Funding

Creation and Repair of Postreplicative DNA GapsRM1GM130450 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI Michael M. Cox, MYRON GOODMAN · 2019 to 2026
$10.4M
NIGMS NIH HHS RM1 GM130450
6 · The paper itself

Abstract

DNA lesions or other barriers frequently compromise replisome progress. The SF2 helicase RecG is a key enzyme in the processing of postreplication gaps or regressed forks in Escherichia coli. A deletion of the recG gene renders cells highly sensitive to a range of DNA damaging agents. Here, we demonstrate that RecG function is at least partially complemented by another SF2 helicase, RadD. A ΔrecGΔradD double mutant exhibits an almost complete growth defect, even in the absence of stress. Suppressors appear quickly, primarily mutations that compromise priA helicase function or recA promoter mutations that reduce recA expression. Deletions of uup (encoding the UvrA-like ABC system Uup), recO, or recF also suppress the ΔrecGΔradD growth phenotype. RadD and RecG appear to avoid toxic situations in DNA metabolism, either resolving or preventing the appearance of DNA repair intermediates produced by RecA or RecA-independent template switching at stalled forks or postreplication gaps. Barriers to replisome progress that require intervention by RadD or RecG occur in virtually every replication cycle. The results highlight the importance of the RadD protein for general chromosome maintenance and repair. They also implicate Uup as a new modulator of RecG function.

Indexed as

Adenosine TriphosphatasesATP-Binding Cassette TransportersDNA, BacterialDNA-Binding ProteinsDNA RepairDNA ReplicationEscherichia coliEscherichia coli ProteinsMutationRecombination, GeneticAdenosine TriphosphatasesATP-Binding Cassette TransportersDNA, BacterialDNA-Binding ProteinsEscherichia coli ProteinsRecG protein, E coliUup protein, E coliYejH protein, E coli

Identifiers

PMID32644157
PMCPMC7470958
OpenAlexW3041800432

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.