Evidence map›Paper›PMID 27257075›Full record

ArticleNucleic acids research2016

A defect in homologous recombination leads to increased translesion synthesis in E. coli.

Karel Naiman, Vincent Pagès, Robert P Fuchs

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Age of Antibiotic Resistance in MDR/XDR Clinical Pathogen ofPharmaceuticals (Basel, Switzerland) · 2023
    Review
  6. Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Targeting evolution of antibiotic resistance by SOS response inhibition.Computational and structural biotechnology journal · 2021
    Review
  15. Article
  16. Lsm12 Mediates Deubiquitination of DNA Polymerase η To HelpApplied and environmental microbiology · 2019
    Article
  17. Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Karel NaimanTeam DNA Damage Tolerance, Cancer Research Center of Marseille (CRCM), CNRS, UMR7258, Marseille, F-13009, France Inserm, U1068, CRCM, Marseille, F-13009, France Institut Paoli-Calmettes, Marseille, F-13009, France Aix-Marseille University, UM 105, F-13284, Marseille, France.
Vincent PagèsTeam DNA Damage Tolerance, Cancer Research Center of Marseille (CRCM), CNRS, UMR7258, Marseille, F-13009, France Inserm, U1068, CRCM, Marseille, F-13009, France Institut Paoli-Calmettes, Marseille, F-13009, France Aix-Marseille University, UM 105, F-13284, Marseille, France vincent.pages@inserm.fr.ORCID 0000-0002-3059-2903
Robert P FuchsTeam DNA Damage Tolerance, Cancer Research Center of Marseille (CRCM), CNRS, UMR7258, Marseille, F-13009, France Inserm, U1068, CRCM, Marseille, F-13009, France Institut Paoli-Calmettes, Marseille, F-13009, France Aix-Marseille University, UM 105, F-13284, Marseille, France robert.fuchs@inserm.fr.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage tolerance pathways allow cells to duplicate their genomes despite the presence of replication blocking lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS) and homology directed gap repair (HDGR). TLS pathways involve specialized DNA polymerases that are able to synthesize past DNA lesions with an intrinsic risk of causing point mutations. In contrast, HDGR pathways are essentially error-free as they rely on the recovery of missing information from the sister chromatid by RecA-mediated homologous recombination. We have investigated the genetic control of pathway choice between TLS and HDGR in vivo in Escherichia coli In a strain with wild type RecA activity, the extent of TLS across replication blocking lesions is generally low while HDGR is used extensively. Interestingly, recA alleles that are partially impaired in D-loop formation confer a decrease in HDGR and a concomitant increase in TLS. Thus, partial defect of RecA's capacity to invade the homologous sister chromatid increases the lifetime of the ssDNA.RecA filament, i.e. the 'SOS signal'. This increase favors TLS by increasing both the TLS polymerase concentration and the lifetime of the TLS substrate, before it becomes sequestered by homologous recombination. In conclusion, the pathway choice between error-prone TLS and error-free HDGR is controlled by the efficiency of homologous recombination.

Indexed as

AllelesDNA, BacterialDNA DamageElectrophoretic Mobility Shift AssayEscherichia coliEscherichia coli ProteinsHomologous RecombinationSOS Response, GeneticsDNA, BacterialEscherichia coli Proteins

Identifiers

PMID27257075
PMCPMC5027485
OpenAlexW2414662560

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.