Evidence map›Paper›PMID 16299390›Full record

ArticleGenetics2006

Differential usage of alternative pathways of double-strand break repair in Drosophila.

Christine R Preston, Carlos C Flores, William R Engels

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 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

58 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
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  11. Hybrid dysgenesis inMobile DNA · 2020
    Article
  12. Gene Knock-Ins inGenetics · 2020
    Article
  13. Article
  14. Article
  15. Article
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  18. Article
  19. Review
  20. 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
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.

Christine R PrestonDepartment of Genetics, University of Wisconsin, Madison, Wisconsin 53706, USA.
Carlos C Flores
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 GM30948NIGMS NIH HHS R01 GM030948NIGMS NIH HHS R56 GM030948
6 · The paper itself

Abstract

Double-strand DNA breaks can be repaired by any of several alternative mechanisms that differ greatly in the nature of the final repaired products. We used a reporter construct, designated "Repair reporter 3" (Rr3), to measure the relative usage of these pathways in Drosophila germ cells. The method works by creating a double-strand break at a specific location such that expression of the red fluorescent protein, DsRed, in the next generation can be used to infer the frequency at which each pathway was used. A key feature of this approach is that most data come from phenotypic scoring, thus allowing large sample sizes and considerable precision in measurements. Specifically, we measured the proportion of breaks repaired by (1) conversion repair, (2) nonhomologous end joining (NHEJ), or (3) single-strand annealing (SSA). For conversion repair, the frequency of mitotic crossing over in the germ line indicates the relative prevalence of repair by double Holliday junction (DHJ) formation vs. the synthesis-dependent strand annealing (SDSA) pathway. We used this method to show that breaks occurring early in germ-line development were much more frequently repaired via single-strand annealing and much less likely to be repaired by end joining compared with identical breaks occurring later in development. Conversion repair was relatively rare when breaks were made either very early or very late in development, but was much more frequent in between. Significantly, the changes in relative usage occurred in a compensatory fashion, such that an increase in one pathway was accompanied by decreases in others. This negative correlation is interpreted to mean that the pathways for double-strand break repair compete with each other to handle a given breakage event.

Indexed as

AnimalsAnimals, Genetically ModifiedCrosses, GeneticDNA, CruciformDNA DamageDNA RepairDrosophila melanogasterFemaleGenes, ReporterLuminescent ProteinsMaleSignal TransductionDNA, Cruciformfluorescent protein 583Luminescent Proteins

Identifiers

PMID16299390
PMCPMC1456205
OpenAlexW2081673572

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.