Evidence map›Paper›PMID 37104614›Full record

ArticleScience (New York, N.Y.)2023

RAD51 bypasses the CMG helicase to promote replication fork reversal.

Wenpeng Liu, Yuichiro Saito, Jessica Jackson, Rahul Bhowmick, Masato T Kanemaki, Alessandro Vindigni, David Cortez

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
14.9field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Wenpeng LiuDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37237 USA.ORCID 0000-0002-2139-4104
Yuichiro SaitoDepartment of Chromosome Science, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Yata 1111, Mishima, Shizuoka 411-8540, Japan.ORCID 0000-0001-5001-0934
Jessica JacksonDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Rahul BhowmickDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37237 USA.
Masato T KanemakiDepartment of Chromosome Science, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Yata 1111, Mishima, Shizuoka 411-8540, Japan.ORCID 0000-0002-7657-1649
Alessandro VindigniDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.ORCID 0000-0002-0568-5067
David CortezDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37237 USA.ORCID 0000-0003-0154-140X
Vanderbilt University · USNational Institute of Genetics · JPWashington University in St. Louis · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI WALTER J. CHAZIN · 2001 to 2026
$89.6M
Analysis of the Replication Stress ResponseR01GM116616 · NIGMS · VANDERBILT UNIVERSITY · PI David K Cortez · 2015 to 2026
$5.4M
Mechanisms of replication fork protection and recoveryR01CA248526 · NCI · WASHINGTON UNIVERSITY · PI Alessandro Vindigni, Lee Zou · 2020 to 2026
$3.6M
Replication fork repriming versus reversalR01CA237263 · NCI · WASHINGTON UNIVERSITY · PI Alessandro Vindigni · 2019 to 2026
$3.0M
NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA237263NCI NIH HHS R01 CA248526NIGMS NIH HHS R01 GM116616
6 · The paper itself

Abstract

Replication fork reversal safeguards genome integrity as a replication stress response. DNA translocases and the RAD51 recombinase catalyze reversal. However, it remains unknown why RAD51 is required and what happens to the replication machinery during reversal. We find that RAD51 uses its strand exchange activity to circumvent the replicative helicase, which remains bound to the stalled fork. RAD51 is not required for fork reversal if the helicase is unloaded. Thus, we propose that RAD51 creates a parental DNA duplex behind the helicase that is used as a substrate by the DNA translocases for branch migration to create a reversed fork structure. Our data explain how fork reversal happens while maintaining the helicase in a position poised to restart DNA synthesis and complete genome duplication.

Indexed as

DNA-Binding ProteinsDNA ReplicationRad51 RecombinaseCarrier ProteinsDNADNA HelicasesHCT116 CellsHumansMinichromosome Maintenance Complex Component 2XenopusCarrier ProteinsDNADNA-Binding ProteinsDNA HelicasesMCM2 protein, humanMinichromosome Maintenance Complex Component 2Rad51 Recombinase

Identifiers

PMID37104614
PMCPMC10302453
OpenAlexW4367173662

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.