Evidence map›Paper›PMID 28407100›Full record

ArticleNucleic acids research2017

SeqA structures behind Escherichia coli replication forks affect replication elongation and restart mechanisms.

Ida Benedikte Pedersen, Emily Helgesen, Ingvild Flåtten, Solveig Fossum-Raunehaug, Kirsten Skarstad

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Replication Fork Breakage and Restart in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2018
    Review
  14. Article
  15. Phenotypes ofJournal of bacteriology · 2017
    Article
  16. 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 1 country.

Ida Benedikte PedersenDepartment of Molecular Cell Biology and Department of Microbiology, Oslo University Hospital, P.O. Box 4950, 0424 Oslo, Norway.
Emily HelgesenDepartment of Molecular Cell Biology and Department of Microbiology, Oslo University Hospital, P.O. Box 4950, 0424 Oslo, Norway.
Ingvild FlåttenDepartment of Molecular Cell Biology and Department of Microbiology, Oslo University Hospital, P.O. Box 4950, 0424 Oslo, Norway.
Solveig Fossum-RaunehaugDepartment of Molecular Cell Biology and Department of Microbiology, Oslo University Hospital, P.O. Box 4950, 0424 Oslo, Norway.
Kirsten SkarstadDepartment of Molecular Cell Biology and Department of Microbiology, Oslo University Hospital, P.O. Box 4950, 0424 Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SeqA protein binds hemi-methylated GATC sites and forms structures that sequester newly replicated origins and trail the replication forks. Cells that lack SeqA display signs of replication fork disintegration. The broken forks could arise because of over-initiation (the launching of too many forks) or lack of dynamic SeqA structures trailing the forks. To confirm one or both of these possible mechanisms, we compared two seqA mutants with the oriCm3 mutant. The oriCm3 mutant over-initiates because of a lack of origin sequestration but has wild-type SeqA protein. Cells with nonfunctional SeqA, but not oriCm3 mutant cells, had problems with replication elongation, were highly dependent on homologous recombination, and exhibited extensive chromosome fragmentation. The results indicate that replication forks frequently break in the absence of SeqA function and that the broken forks are rescued by homologous recombination. We suggest that SeqA may act in two ways to stabilize replication forks: (i) by enabling vital replication fork repair and restarting reactions and (ii) by preventing replication fork rear-end collisions.

Indexed as

DNA ReplicationBacterial Outer Membrane ProteinsDNA, BacterialDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA FragmentationEscherichia coliEscherichia coli ProteinsKineticsMicrobial ViabilityNucleic Acid ConformationBacterial Outer Membrane ProteinsDNA, BacterialDNA-Binding ProteinsEscherichia coli ProteinsSeqA protein, E coli

Identifiers

PMID28407100
PMCPMC5499823
OpenAlexW2606857325

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.