Evidence map›Paper›PMID 29255195›Full record

ArticleNature communications2017

Single-molecule imaging reveals multiple pathways for the recruitment of translesion polymerases after DNA damage.

Elizabeth S Thrall, James E Kath, Seungwoo Chang, Joseph J Loparo

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. 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 12% 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, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. "ThebioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023
    Review
  14. Replication stalling activates SSB for recruitment of DNA damage tolerance factors.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Article
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  20. 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

4 authors at 1 institution in 1 country.

Elizabeth S ThrallDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 250 Longwood Avenue, Boston, MA, 02115, USA.
James E KathDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 250 Longwood Avenue, Boston, MA, 02115, USA.
Seungwoo ChangDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 250 Longwood Avenue, Boston, MA, 02115, USA.
Joseph J LoparoDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 250 Longwood Avenue, Boston, MA, 02115, USA. joseph_loparo@hms.harvard.edu.
Harvard University · US

Funding

Regulation of translesion synthesis by the bacterial replisomeR01GM114065 · NIGMS · HARVARD MEDICAL SCHOOL · PI LOPARO, JOSEPH J. · 2015 to 2024
$3.0M
Visualizing the Bacterial Replisome at Single-Molecule ResolutionF32GM113516 · NIGMS · HARVARD MEDICAL SCHOOL · PI THRALL, ELIZABETH SIMMONS · 2015 to 2016
$116k
NIGMS NIH HHS F32 GM113516NIGMS NIH HHS R01 GM114065
6 · The paper itself

Abstract

Unrepaired DNA lesions are a potent block to replication, leading to replication fork collapse, double-strand DNA breaks, and cell death. Error-prone polymerases overcome this blockade by synthesizing past DNA lesions in a process called translesion synthesis (TLS), but how TLS polymerases gain access to the DNA template remains poorly understood. In this study, we use particle-tracking PALM to image live Escherichia coli cells containing a functional fusion of the endogenous copy of Pol IV to the photoactivatable fluorescent protein PAmCherry. We find that Pol IV is strongly enriched near sites of replication only upon DNA damage. Surprisingly, we find that the mechanism of Pol IV recruitment is dependent on the type of DNA lesion, and that interactions with proteins other than the processivity factor β play a role under certain conditions. Collectively, these results suggest that multiple interactions, influenced by lesion identity, recruit Pol IV to sites of DNA damage.

Indexed as

DNA DamageDNA RepairDNA, BacterialDNA-Directed DNA PolymeraseDNA ReplicationEscherichia coliEscherichia coli ProteinsMicroscopy, FluorescenceMutationProtein BindingDNA, BacterialDNA-Directed DNA PolymeraseEscherichia coli Proteins

Identifiers

PMID29255195
PMCPMC5735139
OpenAlexW2774792866

What OpenQuestion holds

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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.