Evidence map›Paper›PMID 24268579›Full record

ArticleMolecular cell2013

Dynamics of leading-strand lesion skipping by the replisome.

Joseph T P Yeeles, Kenneth J Marians

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

61 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The RecBC complex protects single-stranded DNA gaps during lesion bypass.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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. Review
  9. Article
  10. Review
  11. Article
  12. Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023
    Review
  13. Article
  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. Smc5/6 Complex Promotes Rad3Molecular and cellular biology · 2022
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

1 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Joseph T P YeelesMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.
Kenneth J MariansMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA. Electronic address: kmarians@sloankettering.edu.
Memorial Sloan Kettering Cancer Center · US

Funding

MECHANISMS OF DNA REPLICATIONR37GM034557 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI MARIANS, KENNETH J · 2001 to 2010
$5.8M
MECHANISMS OF LAGGING STRAND SYNTHESISR01GM034557 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI MARIANS, KENNETH J · 1985 to 2018
$5.7M
NIGMS NIH HHS GM34557NIGMS NIH HHS R01 GM034557NIGMS NIH HHS R37 GM034557
6 · The paper itself

Abstract

The E. coli replisome stalls transiently when it encounters a lesion in the leading-strand template, skipping over the damage by reinitiating replication at a new primer synthesized downstream by the primase. We report here that template unwinding and lagging-strand synthesis continue downstream of the lesion at a reduced rate after replisome stalling, that one replisome is capable of skipping multiple lesions, and that the rate-limiting steps of replication restart involve the synthesis and activation of the new primer downstream. We also find little support for the concept that polymerase uncoupling, where extensive lagging-strand synthesis proceeds downstream in the absence of leading-strand synthesis, involves physical separation of the leading-strand polymerase from the replisome. Instead, our data indicate that extensive uncoupled replication likely results from a failure of the leading-strand polymerase still associated with the DNA helicase and the lagging-strand polymerase that are proceeding downstream to reinitiate synthesis.

Indexed as

DNA DamageDNA Replication TimingBacterial ProteinsDNA, BacterialDnaB HelicasesDNA-Directed DNA PolymeraseDNA Polymerase IIIDNA PrimaseEscherichia coliKineticsMultienzyme ComplexesProtein BindingReplisomesTemplates, GeneticBacterial ProteinsDNA, BacterialDnaB HelicasesdnaB protein, E coliDNA-Directed DNA PolymeraseDNA Polymerase IIIDNA PrimaseDnaX protein, BacteriaMultienzyme ComplexesReplisomes

Identifiers

PMID24268579
PMCPMC3877186
OpenAlexW2025007049

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.