Evidence map›Paper›PMID 26122113›Full record

ArticleMutagenesis2015

Requirement of POL3 and POL4 on non-homologous and microhomology-mediated end joining in rad50/xrs2 mutants of Saccharomyces cerevisiae.

Alvaro Galli, Cecilia Y Chan, Liubov Parfenova, Tiziana Cervelli, Robert H Schiestl

Open access · bronzeAbstract read
In one paragraph

Article in Mutagenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Polymerase δ promotes chromosomal rearrangements and imprecise double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  4. Article
  5. Consider the workhorse: Nonhomologous end-joining in budding yeast.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016
    Review
  6. 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

5 authors at 2 institutions in 2 countries.

Alvaro Galli
Cecilia Y ChanDepartments of Pathology, Environmental Health, and Radiation Oncology, David Geffen School of Medicine at UCLA and UCLA School of Public Health, 71-295 CHS, 650 Charles E. Young Drive South, Los Angeles, CA, USA.
Liubov ParfenovaDepartments of Pathology, Environmental Health, and Radiation Oncology, David Geffen School of Medicine at UCLA and UCLA School of Public Health, 71-295 CHS, 650 Charles E. Young Drive South, Los Angeles, CA, USA.
Tiziana Cervelli
Robert H SchiestlDepartments of Pathology, Environmental Health, and Radiation Oncology, David Geffen School of Medicine at UCLA and UCLA School of Public Health, 71-295 CHS, 650 Charles E. Young Drive South, Los Angeles, CA, USA.
UCLA Health · USIstituto di Fisiologia Clinica · IT

Funding

CHEMISTRY BIOLOGY INTERFACE TRAINING PROGRAMT32GM008496 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MAYNARD, HEATHER D · 1993 to 2019
$6.3M
MECHANISM OF RADIATION INDUCED DELAYED GENOTOXICITYR01CA082473 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SCHIESTL, ROBERT H · 1999 to 2002
$650k
NCI NIH HHS 1 RO1 CA82473NIGMS NIH HHS GM08496NIGMS NIH HHS T32 GM008496
6 · The paper itself

Abstract

Non-homologous end joining (NHEJ) directly joins two broken DNA ends without sequence homology. A distinct pathway called microhomology-mediated end joining (MMEJ) relies on a few base pairs of homology between the recombined DNA. The majority of DNA double-strand breaks caused by endogenous oxygen species or ionizing radiation contain damaged bases that hinder direct religation. End processing is required to remove mismatched nucleotides and fill in gaps during end joining of incompatible ends. POL3 in Saccharomyces cerevisiae encodes polymerase δ that is required for DNA replication and other DNA repair processes. Our previous results have shown that POL3 is involved in gap filling at 3' overhangs in POL4-independent NHEJ. Here, we studied the epistatic interaction between POL3, RAD50, XRS2 and POL4 in NHEJ using a plasmid-based endjoining assay in yeast. We demonstrated that either rad50 or xrs2 mutation is epistatic for end joining of compatible ends in the rad50 pol3-t or xrs2 pol3-t double mutants. However, the pol3-t and rad50 or pol3-t and xrs2 mutants caused an additive decrease in the end-joining efficiency of incompatible ends, suggesting that POL3 and RAD50 or POL3 and XRS2 exhibit independent functions in NHEJ. In the rad50 pol4 mutant, end joining of incompatible ends was not detected. In the rad50 or xrs2 mutants, NHEJ events did not contain any microhomology at the rejoined junctions. The pol3-t mutation restored MMEJ in the rad50 or xrs2 mutant backgrounds. Moreover, we demonstrated that NHEJ of incompatible ends required RAD50 and POL4 more than POL3. In conclusion, POL3 and POL4 have differential functions in NHEJ, independent of the RAD50-mediated repair pathway.

Indexed as

DNA End-Joining RepairDNA-Binding ProteinsDNA Polymerase betaDNA Polymerase IIIDNA RepairMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA-Binding ProteinsDNA Polymerase betaDNA Polymerase IIIPOL3 protein, S cerevisiaePOL4 protein, S cerevisiaeRAD50 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsXRS2 protein, S cerevisiae

Identifiers

PMID26122113
PMCPMC4757936
OpenAlexW1889440124

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.