Evidence map›Paper›PMID 27390022›Full record

ArticlePLoS genetics2016

Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates.

Kenji Keyamura, Kota Arai, Takashi Hishida

Abstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Deep structure-function analysis of the endonuclease Mus81 with dominant mutational scanning.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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.

Kenji KeyamuraDepartment of Life Science, Graduate School of Science, Gakushuin University, Tokyo, Japan.
Kota AraiDepartment of Life Science, Graduate School of Science, Gakushuin University, Tokyo, Japan.ORCID 0000-0002-9752-6599
Takashi HishidaDepartment of Life Science, Graduate School of Science, Gakushuin University, Tokyo, Japan.ORCID 0000-0002-9752-6599

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homologous recombination is an evolutionally conserved mechanism that promotes genome stability through the faithful repair of double-strand breaks and single-strand gaps in DNA, and the recovery of stalled or collapsed replication forks. Saccharomyces cerevisiae ATP-dependent DNA helicase Srs2 (a member of the highly conserved UvrD family of helicases) has multiple roles in regulating homologous recombination. A mutation (srs2K41A) resulting in a helicase-dead mutant of Srs2 was found to be lethal in diploid, but not in haploid, cells. In diploid cells, Srs2K41A caused the accumulation of inter-homolog joint molecule intermediates, increased the levels of spontaneous Rad52 foci, and induced gross chromosomal rearrangements. Srs2K41A lethality and accumulation of joint molecules were suppressed by inactivating Rad51 or deleting the Rad51-interaction domain of Srs2, whereas phosphorylation and sumoylation of Srs2 and its interaction with sumoylated proliferating cell nuclear antigen (PCNA) were not required for lethality. The structure-specific complex of crossover junction endonucleases Mus81 and Mms4 was also required for viability of diploid, but not haploid, SRS2 deletion mutants (srs2Δ), and diploid srs2Δ mus81Δ mutants accumulated joint molecule intermediates. Our data suggest that Srs2 and Mus81-Mms4 have critical roles in preventing the formation of (or in resolving) toxic inter-homolog joint molecules, which could otherwise interfere with chromosome segregation and lead to genetic instability.

Indexed as

Genomic InstabilityRecombination, GeneticChromosome SegregationDiploidyDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesDNA ReplicationEndonucleasesFlap EndonucleasesHaploidyHomologous RecombinationMutationPhosphorylationProliferating Cell Nuclear AntigenRad52 DNA Repair and Recombination ProteinDNA-Binding ProteinsDNA HelicasesEndonucleasesFlap EndonucleasesMMS4 protein, S cerevisiaeMUS81 protein, S cerevisiaeProliferating Cell Nuclear AntigenRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiae

Identifiers

PMID27390022
PMCPMC4936719

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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.