Evidence map›Paper›PMID 15184650›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Interplay between Drosophila Bloom's syndrome helicase and Ku autoantigen during nonhomologous end joining repair of P element-induced DNA breaks.

Bosun Min, Brian T Weinert, Donald C Rio

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Mosaic Analysis inGenetics · 2018
    Review
  5. Review
  6. Drosophila IRBP bZIP heterodimer binds P-element DNA and affects hybrid dysgenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. DNA damage and L1 retrotransposition.Journal of biomedicine & biotechnology · 2006
    Article
  18. Formation of deletions during double-strand break repair in Drosophila DmBlm mutants occurs after strand invasion.Proceedings of the National Academy of Sciences of the United States of America · 2004
    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

3 authors at 1 institution in 1 country.

Bosun MinDepartment of Molecular and Cell Biology, Center for Integrative Genomics, 16 Barker Hall, University of California, Berkeley, CA 94720-3204, USA.
Brian T Weinert
Donald C Rio
University of California, Berkeley · US

Funding

MECHANISMS &REGULATION OF DROSOPHILA P ELMNT TRANSPSTNR01GM048862 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI RIO, DONALD C · 1992 to 2003
$1.4M
NIGMS NIH HHS R01 GM048862NIGMS NIH HHS R01 GM48862-12
6 · The paper itself

Abstract

P transposable elements in Drosophila are mobilized via a cut-and-paste mechanism. The broken DNA ends generated during transposition can be repaired via the homology-directed synthesis-dependent strand annealing or by nonhomologous end joining (NHEJ). Genetic studies have demonstrated an interaction between the gene (mus309, for mutagen-sensitive) encoding the Drosophila Bloom's syndrome helicase homolog (DmBLM) and the Ku70 gene, which is involved in NHEJ. We have used RNA interference (RNAi) to knock down expression of DmBLM and one or both of the Drosophila Ku subunits, DmKu70 or DmKu80. Our results show that upon reduction of DmKu, an increase in small deletions (1-49 bp) and large deletions (>/=50 bp) flanking the site of P element-induced breaks is observed, and a reduction in large deletions at these sites is found upon reduction of DmBLM. Moreover, double RNAi of DmKu and DmBLM results in an increase in small deletions characteristic of the DmKu RNAi and also partially suppresses the reduction in repair efficiency observed with DmKu RNAi. These results suggest that there are DNA double-strand break recognition and/or processing events involving DmKu and DmBLM that, when eliminated by RNAi, lead to deletions. Finally, these results raise the possibility that, unlike the situation in mammals, where BLM appears to function exclusively in the homologous repair pathway, in Drosophila, DmBLM may be directly involved in, or at least influence the double-strand break recognition that leads to the NHEJ repair pathway.

Indexed as

Adenosine TriphosphatasesAnimalsAntigens, NuclearBase SequenceBinding SitesBloom SyndromeDNA-Binding ProteinsDNA DamageDNA HelicasesDNA RepairDNA Transposable ElementsDrosophila melanogasterDrosophila ProteinsGene DeletionGenetic TechniquesKu AutoantigenAdenosine TriphosphatasesAntigens, NuclearBloom syndrome proteinDNA-Binding ProteinsDNA HelicasesDNA Transposable ElementsDrosophila ProteinsKu AutoantigenRecQ Helicases

Identifiers

PMID15184650
PMCPMC428445
OpenAlexW2065912182

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.