Evidence map›Paper›PMID 19424425›Full record

ArticlePLoS genetics2009

Recognition of double strand breaks by a mutator protein (MU2) in Drosophila melanogaster.

Raghuvar Dronamraju, James M Mason

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  6. Arp2/3 and Unc45 maintain heterochromatin stability inExperimental biology and medicine (Maywood, N.J.) · 2019
    Article
  7. Review
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  11. And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
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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.

Raghuvar DronamrajuLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
James M Mason
National Institute of Environmental Health Sciences · US

Funding

TELOMERE STRUCTURE IN DROSOPHILAZ01ES021054 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MASON, JAMES M · 1994 to 2008
$2.2M
Chromatin Structure and DNA RepairZIAES102665 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MASON, JAMES M · 2009 to 2012
$1.6M
Intramural NIH HHS Z01 ES021054
6 · The paper itself

Abstract

Telomere capture, a rare event that stabilizes chromosome breaks, is associated with certain genetic abnormalities in humans. Studies pertaining to the generation, maintenance, and biological effects of telomere formation are limited in metazoans. A mutation, mu2(a), in Drosophila melanogaster decreases the rate of repair of double strand DNA breaks in oocytes, thus leading to chromosomes that have lost a natural telomere and gained a new telomere. Amino acid sequence, domain architecture, and protein interactions suggest that MU2 is an ortholog of human MDC1. The MU2 protein is a component of meiotic recombination foci and localizes to repair foci in S2 cells after irradiation in a manner similar to that of phosphorylated histone variant H2Av. Domain searches indicated that the protein contains an N-terminal FHA domain and a C-terminal tandem BRCT domain. Peptide pull-down studies showed that the BRCT domain interacts with phosphorylated H2Av, while the FHA domain interacts with the complex of MRE11, RAD50, and NBS. A frameshift mutation that eliminates the MU2 BRCT domain decreases the number and size of meiotic phospho-H2Av foci. MU2 is also required for the intra-S checkpoint in eye-antennal imaginal discs. MU2 participates at an early stage in the recognition of DNA damage at a step that is prerequisite for both DNA repair and cell cycle checkpoint control. We propose a model suggesting that neotelomeres may arise when radiation-induced chromosome breaks fail to be repaired, fail to arrest progression through meiosis, and are deposited in the zygote, where cell cycle control is absent and rapid rounds of replication and telomere formation ensue.

Indexed as

DNA Breaks, Double-StrandedAdaptor Proteins, Signal TransducingAnimalsAnimals, Genetically ModifiedCell CycleCell Cycle ProteinsCell LineDNA-Binding ProteinsDNA RepairDrosophila melanogasterDrosophila ProteinsFemaleGenes, InsectHistonesHumansMeiosisAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsDrosophila ProteinsHistonesMDC1 protein, humanMU2 protein, DrosophilaNuclear ProteinsTrans-Activators

Identifiers

PMID19424425
PMCPMC2672170
OpenAlexW2033127565

What OpenQuestion holds

Textmetadata
LicenceCC0
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.