Evidence map›Paper›PMID 16219790›Full record

ArticleGenetics2006

Growth defect and mutator phenotypes of RecQ-deficient Neurospora crassa mutants separately result from homologous recombination and nonhomologous end joining during repair of DNA double-strand breaks.

Akihiro Kato, Hirokazu Inoue

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Remodeling of perturbed chromatin can initiate de novo transcriptional and post-transcriptional silencing.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

2 authors at 1 institution in 1 country.

Akihiro KatoLaboratory of Genetics, Department of Regulation Biology, Faculty of Science, Saitama University, 338-8570 Saitama, Japan.
Hirokazu Inoue
Saitama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RecQ helicases function in the maintenance of genome stability in many organisms. The filamentous fungus Neurospora crassa has two RecQ homologs, QDE3 and RECQ2. We found that the qde-3 recQ2 double mutant showed a severe growth defect. The growth defect was alleviated by mutation in mei-3, the homolog of yeast RAD51, which is required for homologous recombination (HR), suggesting that HR is responsible for this phenotype. We also found that the qde-3 recQ2 double mutant showed a mutator phenotype, yielding mostly deletions. This phenotype was completely suppressed by mutation of mus-52, a homolog of the human KU80 gene that is required for nonhomologous end joining (NHEJ), but was unaffected by mutation of mei-3. The high spontaneous mutation frequency in the double mutant is thus likely to be due to NHEJ acting on an elevated frequency of double-strand breaks (DSBs) and we therefore suggest that QDE3 and RECQ2 maintain chromosome stability by suppressing the formation of spontaneous DSBs.

Indexed as

DNA RepairRecombination, GeneticAdenosine TriphosphatasesAntigens, NuclearChromosome BreakageDNADNA-Binding ProteinsDNA, FungalDNA HelicasesEpistasis, GeneticFungal ProteinsGene DeletionKu AutoantigenMutationNeurospora crassaPhenotypeAdenosine TriphosphatasesAntigens, NuclearDNADNA-Binding ProteinsDNA, FungalDNA HelicasesFungal ProteinsKu AutoantigenMEI-3 protein, Neurospora crassaQDE-3 protein, Neurospora crassaRecQ HelicasesRECQL protein, humanXrcc6 protein, human

Identifiers

PMID16219790
PMCPMC1456140
OpenAlexW2032365059

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.