Evidence map›Paper›PMID 26684201›Full record

ArticlePLoS genetics2015

The Eukaryotic Mismatch Recognition Complexes Track with the Replisome during DNA Synthesis.

Joanna E Haye, Alison E Gammie

Abstract read
In one paragraph

Article in PLoS genetics, 2015. 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. DNA Repair Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. Article
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  5. Review
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  14. Replicating repetitive DNA.Nature cell biology · 2016
    Article
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.

Joanna E HayeDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Alison E GammieDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Tracie Saunders · 1997 to 2026
$94.5M
Spatial Patterning During DevelopmentP50GM071508 · NIGMS · PRINCETON UNIVERSITY · PI GAMMIE, ALISON E · 2004 to 2013
$30.6M
PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
Quantitavie and Computational Biology Graduate ProgramT32HG003284 · NHGRI · PRINCETON UNIVERSITY · PI Joshua Michael Akey, Stanislav Y. Shvartsman · 2004 to 2026
$9.9M
Mechanisms of Nuclear and Cell Fusion in YeastR01GM037739 · NIGMS · PRINCETON UNIVERSITY · PI ROSE, MARK DAVID · 1987 to 2016
$7.4M
NCI NIH HHS P30 CA072720NHGRI NIH HHS T32 HG003284NIGMS NIH HHS P50 GM071508NIGMS NIH HHS R01 GM037739NIGMS NIH HHS T32 GM007388
6 · The paper itself

Abstract

During replication, mismatch repair proteins recognize and repair mispaired bases that escape the proofreading activity of DNA polymerase. In this work, we tested the model that the eukaryotic mismatch recognition complex tracks with the advancing replisome. Using yeast, we examined the dynamics during replication of the leading strand polymerase Polε using Pol2 and the eukaryotic mismatch recognition complex using Msh2, the invariant protein involved in mismatch recognition. Specifically, we synchronized cells and processed samples using chromatin immunoprecipitation combined with custom DNA tiling arrays (ChIP-chip). The Polε signal was not detectable in G1, but was observed at active origins and replicating DNA throughout S-phase. The Polε signal provided the resolution to track origin firing timing and efficiencies as well as replisome progression rates. By detecting Polε and Msh2 dynamics within the same strain, we established that the mismatch recognition complex binds origins and spreads to adjacent regions with the replisome. In mismatch repair defective PCNA mutants, we observed that Msh2 binds to regions of replicating DNA, but the distribution and dynamics are altered, suggesting that PCNA is not the sole determinant for the mismatch recognition complex association with replicating regions, but may influence the dynamics of movement. Using biochemical and genomic methods, we provide evidence that both MutS complexes are in the vicinity of the replisome to efficiently repair the entire spectrum of mutations during replication. Our data supports the model that the proximity of MutSα/β to the replisome for the efficient repair of the newly synthesized strand before chromatin reassembles.

Indexed as

DNADNA-Directed DNA PolymeraseDNA Mismatch RepairDNA Polymerase IIDNA RepairDNA ReplicationMutationMutS DNA Mismatch-Binding ProteinMutS Homolog 2 ProteinSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNADNA-Directed DNA PolymeraseDNA Polymerase IIMSH2 protein, S cerevisiaeMutS DNA Mismatch-Binding ProteinMutS Homolog 2 ProteinSaccharomyces cerevisiae Proteins

Identifiers

PMID26684201
PMCPMC4684283

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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.