Evidence map›Paper›PMID 14612428›Full record

ArticleMolecular and cellular biology2003

Yeast Rad52 and Rad51 recombination proteins define a second pathway of DNA damage assessment in response to a single double-strand break.

Sang Eun Lee, Achille Pellicioli, Moreshwar B Vaze, Neal Sugawara, Anna Malkova, Marco Foiani, James E Haber

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. DNA damage checkpoint triggers autophagy to regulate the initiation of anaphase.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
  18. Review
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

Sang Eun LeeRosenstiel Center and Department of Biology, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
Achille Pellicioli
Moreshwar B Vaze
Neal Sugawara
Anna Malkova
Marco Foiani
James E Haber
Brandeis University · USUniversity of Milan · IT

Funding

Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
Arrest, Recovery, and Adaptation from DNA DamageR01GM061766 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2001 to 2016
$4.6M
RECOMBINATION MECHANISMS IN YEAST CELL DIFFERENTIATIONR01GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 1985 to 2006
$3.4M
NIGMS NIH HHS GM20056NIGMS NIH HHS GM61766NIGMS NIH HHS R01 GM020056NIGMS NIH HHS R01 GM061766NIGMS NIH HHS R37 GM020056
6 · The paper itself

Abstract

Saccharomyces cells with a single unrepaired double-strand break adapt after checkpoint-mediated G(2)/M arrest. We have found that both Rad51 and Rad52 recombination proteins play key roles in adaptation. Cells lacking Rad51p fail to adapt, but deleting RAD52 suppresses rad51Delta. rad52Delta also suppresses adaptation defects of srs2Delta mutants but not those of yku70Delta or tid1Delta mutants. Neither rad54Delta nor rad55Delta affects adaptation. A Rad51 mutant that fails to interact with Rad52p is adaptation defective; conversely, a C-terminal truncation mutant of Rad52p, impaired in interaction with Rad51p, is also adaptation defective. In contrast, rad51-K191A, a mutation that abolishes recombination and results in a protein that does not bind to single-stranded DNA (ssDNA), supports adaptation, as do Rad51 mutants impaired in interaction with Rad54p or Rad55p. An rfa1-t11 mutation in the ssDNA binding complex RPA partially restores adaptation in rad51Delta mutants and fully restores adaptation in yku70Delta and tid1Delta mutants. Surprisingly, although neither rfa1-t11 nor rad52Delta mutants are adaptation defective, the rad52Delta rfa1-t11 double mutant fails to adapt and exhibits the persistent hyperphosphorylation of the DNA damage checkpoint protein Rad53 after HO induction. We suggest that monitoring of the extent of DNA damage depends on independent binding of RPA and Rad52p to ssDNA, with Rad52p's activity modulated by Rad51p whereas RPA's action depends on Tid1p.

Indexed as

Cell Cycle ProteinsDNA DamageBase SequenceCell CycleCheckpoint Kinase 2DNA-Binding ProteinsDNA, FungalDNA RepairDNA, Single-StrandedEpistasis, GeneticGenes, FungalMutationPhosphorylationProtein Serine-Threonine KinasesRad52 DNA Repair and Recombination ProteinRecombinant ProteinsCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsDNA, FungalDNA, Single-StrandedProtein Serine-Threonine KinasesRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeRAD53 protein, S cerevisiaeRecombinant ProteinsSaccharomyces cerevisiae Proteins

Identifiers

PMID14612428
PMCPMC262690
OpenAlexW2096219875

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.