Evidence map›Paper›PMID 25731766›Full record

ReviewCold Spring Harbor perspectives in biology2015

Mismatch repair during homologous and homeologous recombination.

Maria Spies, Richard Fishel

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing 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

111 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
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  8. Article
  9. Therapeutic targeting of mismatch repair-deficient cancers.Nature reviews. Clinical oncology · 2025
    Review
  10. Article
  11. Homology-arm length of donor DNA affects the impact of Msh2 loss on homologous recombination-mediated gene targeting.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

51 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

2 authors.

Maria SpiesDepartment of Biochemistry, University of Iowa, Iowa City, Iowa 52242.
Richard FishelDepartment of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University Medical Center and Comprehensive Cancer Center, Columbus, Ohio 43210 Human Genetics Institute, The Ohio State University Medical Center, Columbus, Ohio 43210 Physics Department, The Ohio State University, Columbus, Ohio 43210.

Funding

The Human Mismatch Repair Proteins and CarcinogenesisR01CA067007 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI Richard Fishel · 1995 to 2026
$9.6M
Regulation of unwinding and remodeling activities in FeS-DNA helicasesR01GM108617 · NIGMS · UNIVERSITY OF IOWA · PI SPIES, MARIA · 2014 to 2018
$1.6M
NCI NIH HHS CA67007NCI NIH HHS R01 CA067007NIGMS NIH HHS GM108617NIGMS NIH HHS R01 GM108617
6 · The paper itself

Abstract

Homologous recombination (HR) and mismatch repair (MMR) are inextricably linked. HR pairs homologous chromosomes before meiosis I and is ultimately responsible for generating genetic diversity during sexual reproduction. HR is initiated in meiosis by numerous programmed DNA double-strand breaks (DSBs; several hundred in mammals). A characteristic feature of HR is the exchange of DNA strands, which results in the formation of heteroduplex DNA. Mismatched nucleotides arise in heteroduplex DNA because the participating parental chromosomes contain nonidentical sequences. These mismatched nucleotides may be processed by MMR, resulting in nonreciprocal exchange of genetic information (gene conversion). MMR and HR also play prominent roles in mitotic cells during genome duplication; MMR rectifies polymerase misincorporation errors, whereas HR contributes to replication fork maintenance, as well as the repair of spontaneous DSBs and genotoxic lesions that affect both DNA strands. MMR suppresses HR when the heteroduplex DNA contains excessive mismatched nucleotides, termed homeologous recombination. The regulation of homeologous recombination by MMR ensures the accuracy of DSB repair and significantly contributes to species barriers during sexual reproduction. This review discusses the history, genetics, biochemistry, biophysics, and the current state of studies on the role of MMR in homologous and homeologous recombination from bacteria to humans.

Indexed as

Biological EvolutionDNA Breaks, Double-StrandedModels, BiologicalAnimalsDNA Mismatch RepairHomologous RecombinationHumansMeiosisSpecies Specificity

Identifiers

PMID25731766
PMCPMC4355274

What OpenQuestion holds

Textmetadata
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.