Evidence map›Paper›PMID 22912599›Full record

ArticlePLoS genetics2012

Components of a Fanconi-like pathway control Pso2-independent DNA interstrand crosslink repair in yeast.

Thomas A Ward, Zuzana Dudášová, Sovan Sarkar, Mangesh R Bhide, Danuša Vlasáková, Miroslav Chovanec, Peter J McHugh

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.Progress in biophysics and molecular biology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Organization and dynamics of yeast mitochondrial nucleoids.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  15. Mgm101: A double-duty Rad52-like protein.Cell cycle (Georgetown, Tex.) · 2016
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

7 authors at 4 institutions in 3 countries.

Thomas A WardDepartment of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Zuzana Dudášová
Sovan Sarkar
Mangesh R Bhide
Danuša Vlasáková
Miroslav Chovanec
Peter J McHugh
Laboratory of Molecular Genetics · PLUniversity of Oxford · GBJohn Radcliffe Hospital · GBUniversity of Veterinary Medicine in Košice · SK

Funding

Cancer Research UK CA9047/A10111
6 · The paper itself

Abstract

Fanconi anemia (FA) is a devastating genetic disease, associated with genomic instability and defects in DNA interstrand cross-link (ICL) repair. The FA repair pathway is not thought to be conserved in budding yeast, and although the yeast Mph1 helicase is a putative homolog of human FANCM, yeast cells disrupted for MPH1 are not sensitive to ICLs. Here, we reveal a key role for Mph1 in ICL repair when the Pso2 exonuclease is inactivated. We find that the yeast FANCM ortholog Mph1 physically and functionally interacts with Mgm101, a protein previously implicated in mitochondrial DNA repair, and the MutSα mismatch repair factor (Msh2-Msh6). Co-disruption of MPH1, MGM101, MSH6, or MSH2 with PSO2 produces a lesion-specific increase in ICL sensitivity, the elevation of ICL-induced chromosomal rearrangements, and persistence of ICL-associated DNA double-strand breaks. We find that Mph1-Mgm101-MutSα directs the ICL-induced recruitment of Exo1 to chromatin, and we propose that Exo1 is an alternative 5'-3' exonuclease utilised for ICL repair in the absence of Pso2. Moreover, ICL-induced Rad51 chromatin loading is delayed when both Pso2 and components of the Mph1-Mgm101-MutSα and Exo1 pathway are inactivated, demonstrating that the homologous recombination stages of ICL repair are inhibited. Finally, the FANCJ- and FANCP-related factors Chl1 and Slx4, respectively, are also components of the genetic pathway controlled by Mph1-Mgm101-MutSα. Together this suggests that a prototypical FA-related ICL repair pathway operates in budding yeast, which acts redundantly with the pathway controlled by Pso2, and is required for the targeting of Exo1 to chromatin to execute ICL repair.

Indexed as

DNA RepairChromosomal Proteins, Non-HistoneDEAD-box RNA HelicasesDNA-Binding ProteinsDNA Breaks, Double-StrandedEndodeoxyribonucleasesExodeoxyribonucleasesFanconi AnemiaHumansMitochondrial ProteinsModels, BiologicalMutS Homolog 2 ProteinSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionCHL1 protein, S cerevisiaeChromosomal Proteins, Non-HistoneDEAD-box RNA HelicasesDNA-Binding ProteinsEndodeoxyribonucleasesexodeoxyribonuclease IExodeoxyribonucleasesMGM101 protein, S cerevisiaeMitochondrial ProteinsMPH1 protein, S cerevisiaeMSH2 protein, S cerevisiaeMSH6 protein, S cerevisiaeMutS Homolog 2 ProteinPSO2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSLX4 protein, S cerevisiae

Identifiers

PMID22912599
PMCPMC3415447
OpenAlexW2121150109

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.