Evidence map›Paper›PMID 17075047›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Template disruptions and failure of double Holliday junction dissolution during double-strand break repair in Drosophila BLM mutants.

Dena Johnson-Schlitz, William R Engels

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Holliday junction resolvases.Cold Spring Harbor perspectives in biology · 2014
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Genome-wide analyses of Geraniaceae plastid DNA reveal unprecedented patterns of increased nucleotide substitutions.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  17. Cleavage mechanism of human Mus81-Eme1 acting on Holliday-junction structures.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  18. Article
  19. Article
  20. Two closely related RecQ helicases have antagonistic roles in homologous recombination and DNA repair in Arabidopsis thaliana.Proceedings of the National Academy of Sciences of the United States of America · 2007
    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

2 authors at 1 institution in 1 country.

Dena Johnson-SchlitzGenetics Department, University of Wisconsin, Madison, WI 53706, USA.
William R Engels
University of Wisconsin–Madison · US

Funding

TRANSPOSITION AND DNA REPAIR IN DROSOPHILAR01GM030948 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI ENGELS, WILLIAM R. · 1985 to 2011
$5.2M
DNA Repair and Aging in DrosophilaR56GM030948 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI ENGELS, WILLIAM R. · 2007 to 2007
$490k
NIGMS NIH HHS GM 30948NIGMS NIH HHS R01 GM030948NIGMS NIH HHS R56 GM030948
6 · The paper itself

Abstract

Previous biochemical studies of the BLM gene product have shown its ability in conjunction with topoisomerase IIIalpha to resolve double Holliday structures through a process called "dissolution." This process could prevent crossing over during repair of double-strand breaks. We report an analysis of the Drosophila BLM gene, DmBlm, in the repair of double-strand breaks in the premeiotic germ line of Drosophila males. With a repair reporter construct, Rr3, and other genetic tools, we show that DmBlm mutants are defective for homologous repair but show a compensating increase in single-strand annealing. Increases of 40- to 50-fold in crossing over and flanking deletions also were seen. Perhaps most significantly, the template used for homologous repair in DmBlm mutants is itself subject to deletions and complex rearrangements. These template disruptions are indicative of failure to resolve double Holliday junctions. These findings, along with the demonstration that a weak allele of topoisomerase IIIalpha has some of the same defects as DmBlm, support the dissolution model. Finally, an analysis of DmBlm mutants in conjunction with mus81 or spnA (Rad51) reveals a second function of BLM distinct from the repair of induced double-strand breaks and possibly related to maintenance of replication forks.

Indexed as

DNA Breaks, Double-StrandedGenes, InsectMutationAnimalsBase SequenceDNADNA, CruciformDNA HelicasesDNA RepairDrosophila melanogasterDrosophila ProteinsFemaleMaleMeiosisMolecular Sequence DataPhenotypeblm protein, DrosophilaDNADNA, CruciformDNA HelicasesDrosophila ProteinsRad51 Recombinasespn-A protein, Drosophila

Identifiers

PMID17075047
PMCPMC1636541
OpenAlexW2143129370

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.