Evidence map›Paper›PMID 25699708›Full record

ArticleMolecular cell2015

Top3-Rmi1 dissolve Rad51-mediated D loops by a topoisomerase-based mechanism.

Clare L Fasching, Petr Cejka, Stephen C Kowalczykowski, Wolf-Dietrich Heyer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

92 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
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  4. Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
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32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Clare L FaschingDepartment of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA.
Petr CejkaDepartment of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA.
Stephen C KowalczykowskiDepartment of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA; Department of Molecular & Cellular Biology, University of California, Davis, Davis, CA 95616-8665, USA.
Wolf-Dietrich HeyerDepartment of Microbiology & Molecular Genetics, University of California, Davis, Davis, CA 95616-8665, USA; Department of Molecular & Cellular Biology, University of California, Davis, Davis, CA 95616-8665, USA. Electronic address: wdheyer@ucdavis.edu.
University of California, Davis · US

Funding

RECOMBINATIONAL MECHANISMS OF DNA REPAIR IN EUKARYOTESR01GM058015 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2000 to 2025
$8.8M
Biochemical Mechanisms and Function of DNA HelicasesR01GM041347 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI KOWALCZYKOWSKI, STEPHEN CHARLES · 1989 to 2018
$7.6M
Regulation of Recombinational DNA RepairR01CA092276 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2001 to 2020
$5.2M
Mechanistic Studies of Genetic RecombinationR01GM062653 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KOWALCZYKOWSKI, STEPHEN CHARLES · 2010 to 2018
$4.4M
MECHANISTIC STUDIES OF GENETIC RECOMBINATIONR37GM062653 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI KOWALCZYKOWSKI, STEPHEN CHARLES · 2000 to 2009
$3.6M
Functions of Rad51 Paralogs in Recombinational DNA RepairR01CA154920 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH, KOWALCZYKOWSKI, STEPHEN CHARLES · 2011 to 2015
$2.6M
Role of Sgs1 in homologous recombination: Dissolution of branched DNA substratesF32GM083509 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FASCHING, CLARE L · 2008 to 2010
$149k
NCI NIH HHS CA154920NCI NIH HHS CA92276NCI NIH HHS R01 CA092276NCI NIH HHS R01 CA154920NIGMS NIH HHS F32 GM083509NIGMS NIH HHS F32 GM83509NIGMS NIH HHS GM41347NIGMS NIH HHS GM58015NIGMS NIH HHS GM62653NIGMS NIH HHS R01 GM041347NIGMS NIH HHS R01 GM058015NIGMS NIH HHS R01 GM062653NIGMS NIH HHS R37 GM062653
6 · The paper itself

Abstract

The displacement loop (D loop) is a DNA strand invasion product formed during homologous recombination. Disruption of nascent D loops prevents recombination, and during synthesis-dependent strand annealing (SDSA), disruption of D loops extended by DNA polymerase ensures a non-crossover outcome. The proteins implicated in D loop disruption are DNA motor proteins/helicases that act by moving DNA junctions. Here we report that D loops can also be disrupted by DNA topoisomerase 3 (Top3), and this disruption depends on Top3's catalytic activity. Yeast Top3 specifically disrupts D loops mediated by yeast Rad51/Rad54; protein-free D loops or D loop mediated by bacterial RecA protein or human RAD51/RAD54 resist dissolution. Also, the human Topoisomerase IIIa-RMI1-RMI2 complex is capable of dissolving D loops. Consistent with genetic data, we suggest that the extreme growth defect and hyper-recombination phenotype of Top3-deficient yeast cells is partially a result of unprocessed D loops.

Indexed as

Models, GeneticDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesHomologous RecombinationHumansRad51 RecombinaseRecQ HelicasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpecies SpecificityDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesRAD51 protein, S cerevisiaeRad51 RecombinaseRAD54 protein, S cerevisiaeRecQ HelicasesRmi1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTOP3 protein, S cerevisiae

Identifiers

PMID25699708
PMCPMC4338411
OpenAlexW2128948249

What OpenQuestion holds

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Registered trials

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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.