Evidence map›Paper›PMID 23858457›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Homologous recombination rescues ssDNA gaps generated by nucleotide excision repair and reduced translesion DNA synthesis in yeast G2 cells.

Wenjian Ma, James W Westmoreland, Michael A Resnick

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Long repeating (TTAGGG)The Journal of biological chemistry · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
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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 at 2 institutions in 1 country.

Wenjian MaChromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
James W Westmoreland
Michael A Resnick
National Institutes of Health · USNational Institute of Environmental Health Sciences · US

Funding

Mechanisms Of Genome InstabilityZIAES065073 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 2009 to 2014
$9.3M
Double Strand Break Repair And RecombinationZIAES021016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2018
$5.6M
MOLECULAR MECHANISMS OF DNA REPAIR AND RECOMBINATION IN YEASTZ01ES065073 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1991 to 2008
$2.8M
Intramural NIH HHS Z01 ES065073
6 · The paper itself

Abstract

Repair of DNA bulky lesions often involves multiple repair pathways such as nucleotide-excision repair, translesion DNA synthesis (TLS), and homologous recombination (HR). Although there is considerable information about individual pathways, little is known about the complex interactions or extent to which damage in single strands, such as the damage generated by UV, can result in double-strand breaks (DSBs) and/or generate HR. We investigated the consequences of UV-induced lesions in nonreplicating G2 cells of budding yeast. In contrast to WT cells, there was a dramatic increase in ssDNA gaps for cells deficient in the TLS polymerases η (Rad30) and ζ (Rev3). Surprisingly, repair in TLS-deficient G2 cells required HR repair genes RAD51 and RAD52, directly revealing a redundancy of TLS and HR functions in repair of ssDNAs. Using a physical assay that detects recombination between circular sister chromatids within a few hours after UV, we show an approximate three-fold increase in recombinants in the TLS mutants over that in WT cells. The recombination, which required RAD51 and RAD52, does not appear to be caused by DSBs, because a dose of ionizing radiation producing 20 times more DSBs was much less efficient than UV in producing recombinants. Thus, in addition to revealing TLS and HR functional redundancy, we establish that UV-induced recombination in TLS mutants is not attributable to DSBs. These findings suggest that ssDNA that might originate during the repair of closely opposed lesions or of ssDNA-containing lesions or from uncoupled replication may drive recombination directly in various species, including humans.

Indexed as

Ultraviolet RaysDNA Breaks, Single-StrandedDNA, FungalDNA RepairDNA, Single-StrandedG2 PhaseHumansSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA, FungalDNA, Single-StrandedSaccharomyces cerevisiae Proteins

Identifiers

PMID23858457
PMCPMC3732972
OpenAlexW2076339637

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.