Evidence map›Paper›PMID 26003632›Full record

ReviewDNA repair2015

RecBCD is required to complete chromosomal replication: Implications for double-strand break frequencies and repair mechanisms.

Justin Courcelle, Brian M Wendel, Dena D Livingstone, Charmain T Courcelle

Abstract readReview
In one paragraph

Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  11. The methylation-independent mismatch repair machinery inMicrobiology (Reading, England) · 2021
    Review
  12. Article
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  20. Nontarget Biomolecules Alter Macromolecular Changes Induced by Bactericidal Low-Temperature Plasma.IEEE transactions on radiation and plasma medical sciences · 2018
    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

4 authors at 1 institution in 1 country.

Justin CourcelleDepartment of Biology, Portland State University, Portland, OR 97201, United States. Electronic address: justc@pdx.edu.
Brian M WendelDepartment of Biology, Portland State University, Portland, OR 97201, United States.
Dena D LivingstoneDepartment of Biology, Portland State University, Portland, OR 97201, United States.
Charmain T CourcelleDepartment of Biology, Portland State University, Portland, OR 97201, United States.
Portland State University · US

Funding

Mechanism of DNA interstrand crosslink repair in vivoR15ES025953 · NIEHS · PORTLAND STATE UNIVERSITY · PI COURCELLE, JUSTIN · 2015 to 2015
$446k
R15 AREA: Replication in the Presence of Oxidative DNA damageR15ES021594 · NIEHS · PORTLAND STATE UNIVERSITY · PI COURCELLE, JUSTIN · 2012 to 2012
$437k
Transcription-coupled repair of Oxidative DNA damage in vivoR21ES018940 · NIEHS · PORTLAND STATE UNIVERSITY · PI COURCELLE, JUSTIN · 2010 to 2011
$398k
NIEHS NIH HHS R15 ES021594NIEHS NIH HHS R15 ES025953NIEHS NIH HHS R15ES025953NIEHS NIH HHS R21 ES018940
6 · The paper itself

Abstract

Several aspects of the mechanism of homologous double-strand break repair remain unclear. Although intensive efforts have focused on how recombination reactions initiate, far less is known about the molecular events that follow. Based upon biochemical studies, current models propose that RecBCD processes double-strand ends and loads RecA to initiate recombinational repair. However, recent studies have shown that RecBCD plays a critical role in completing replication events on the chromosome through a mechanism that does not involve RecA or recombination. Here, we examine several studies, both early and recent, that suggest RecBCD also operates late in the recombination process - after initiation, strand invasion, and crossover resolution have occurred. Similar to its role in completing replication, we propose a model in which RecBCD is required to resect and resolve the DNA synthesis associated with homologous recombination at the point where the missing sequences on the broken molecule have been restored. We explain how the impaired ability to complete chromosome replication in recBC and recD mutants is likely to account for the loss of viability and genome instability in these mutants, and conclude that spontaneous double-strand breaks and replication fork collapse occur far less frequently than previously speculated.

Indexed as

Gene Expression Regulation, BacterialRecombinational DNA RepairChromosomes, BacterialDNA, BacterialDNA Breaks, Double-StrandedDNA ReplicationEscherichia coliEscherichia coli ProteinsExodeoxyribonuclease VGenomic InstabilityHomologous RecombinationRec A RecombinasesSignal TransductionDNA, BacterialEscherichia coli ProteinsExodeoxyribonuclease Vexodeoxyribonuclease V, E coliRec A RecombinasesDouble-strand break repairHomologous recombinationRecBCDReplication completion

Identifiers

PMID26003632
PMCPMC4522357
OpenAlexW2008343350

What OpenQuestion holds

Textmetadata
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.