Evidence map›Paper›PMID 28781165›Full record

ArticleCell2017

Multi-invasions Are Recombination Byproducts that Induce Chromosomal Rearrangements.

Aurèle Piazza, William Douglass Wright, Wolf-Dietrich Heyer

Abstract read
In one paragraph

Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
–field-weighted citation impact
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

84 citing papers in PubMed.

  1. Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. RAD51AP1 is a versatile RAD51 modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Chromothripsis.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  15. Review
  16. Article
  17. Molecular basis of FIGNL1 in dissociating RAD51 from DNA and chromatin.bioRxiv : the preprint server for biology · 2024
    Article
  18. Article
  19. Article
  20. Article

24 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

3 authors.

Aurèle PiazzaDepartment of Microbiology and Molecular Genetics, One Shields Avenue, University of California, Davis, Davis, CA 95616, USA.
William Douglass WrightDepartment of Microbiology and Molecular Genetics, One Shields Avenue, University of California, Davis, Davis, CA 95616, USA.
Wolf-Dietrich HeyerDepartment of Microbiology and Molecular Genetics, One Shields Avenue, University of California, Davis, Davis, CA 95616, USA; Department of Molecular and Cellular Biology, One Shields Avenue, University of California, Davis, Davis, CA 95616, USA. Electronic address: wdheyer@ucdavis.edu.

Funding

RECOMBINATIONAL MECHANISMS OF DNA REPAIR IN EUKARYOTESR01GM058015 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2000 to 2025
$8.8M
Regulation of Recombinational DNA RepairR01CA092276 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2001 to 2020
$5.2M
NCI NIH HHS R01 CA092276NIGMS NIH HHS R01 GM058015
6 · The paper itself

Abstract

Inaccurate repair of broken chromosomes generates structural variants that can fuel evolution and inflict pathology. We describe a novel rearrangement mechanism in which translocation between intact chromosomes is induced by a lesion on a third chromosome. This multi-invasion-induced rearrangement (MIR) stems from a homologous recombination byproduct, where a broken DNA end simultaneously invades two intact donors. No homology is required between the donors, and the intervening sequence from the invading molecule is inserted at the translocation site. MIR is stimulated by increasing homology length and spatial proximity of the donors and depends on the overlapping activities of the structure-selective endonucleases Mus81-Mms4, Slx1-Slx4, and Yen1. Conversely, the 3'-flap nuclease Rad1-Rad10 and enzymes known to disrupt recombination intermediates (Sgs1-Top3-Rmi1, Srs2, and Mph1) inhibit MIR. Resolution of MIR intermediates propagates secondary chromosome breaks that frequently cause additional rearrangements. MIR features have implications for the formation of simple and complex rearrangements underlying human pathologies.

Indexed as

DNA RepairGenomic InstabilityTranslocation, GeneticChromosomesDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA, Single-StrandedHomologous RecombinationHumansSaccharomyces cerevisiaeDNA-Binding ProteinsDNA, Single-StrandedchromothripsisD-loopendonucleasegenomic instabilityhelicasehomologous recombinationhomology searchmulti-invasiontranslocation

Identifiers

PMID28781165
PMCPMC5554464

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.