Evidence map›Paper›PMID 19102749›Full record

ArticleBMC developmental biology2008

Pleiotropic effects in Eya3 knockout mice.

Torben Söker, Claudia Dalke, Oliver Puk, Thomas Floss, Lore Becker, Ines Bolle, Jack Favor, Wolfgang Hans, Sabine M Hölter, Marion Horsch and 18 more

Open access · hybridAbstract read
In one paragraph

Article in BMC developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Eya2 expression during mouse embryonic development revealed by Eya2Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  8. Review
  9. Article
  10. Review
  11. Multiple Retinal Anomalies in Wfs1-Deficient Mice.Diagnostics (Basel, Switzerland) · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Transcriptional regulation of cranial sensory placode development.Current topics in developmental biology · 2015
    Review
  17. Review
  18. The Eyes Absent proteins in development and disease.Cellular and molecular life sciences : CMLS · 2013
    Review
  19. Atypical protein phosphatases: emerging players in cellular signaling.International journal of molecular sciences · 2013
    Article
  20. 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

28 authors at 5 institutions in 1 country.

Torben SökerHelmholtz Center Munich, German Research Center for Environmental Health, Institute of Developmental Genetics, Neuherberg, Germany. tsoeker@web.de
Claudia Dalke
Oliver Puk
Thomas Floss
Lore Becker
Ines Bolle
Jack Favor
Wolfgang Hans
Sabine M Hölter
Marion Horsch
Magdalena Kallnik
Eva Kling
Corinna Moerth
Anja Schrewe
Christian Stigloher
Stefanie Topp
Valerie Gailus-Durner
Beatrix Naton
Johannes Beckers
Helmut Fuchs
Boris Ivandic
Thomas Klopstock
Holger Schulz
Eckhard Wolf
Wolfgang Wurst
Laure Bally-Cuif
Martin Hrabé de Angelis
Jochen Graw
Helmholtz Zentrum München · DEEuropean Molecular Biology Organization · DELudwig-Maximilians-Universität München · DETechnical University of Munich · DEWeihenstephan-Triesdorf University of Applied Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn Drosophila, mutations in the gene eyes absent (eya) lead to severe defects in eye development. The functions of its mammalian orthologs Eya1-4 are only partially understood and no mouse model exists for Eya3. Therefore, we characterized the phenotype of a new Eya3 knockout mouse mutant.

resultsExpression analysis of Eya3 by in-situ hybridizations and beta-Gal-staining of Eya3 mutant mice revealed abundant expression of the gene throughout development, e.g. in brain, eyes, heart, somites and limbs suggesting pleiotropic effects of the mutated gene. A similar complex expression pattern was observed also in zebrafish embryos. The phenotype of young adult Eya3 mouse mutants was systematically analyzed within the German Mouse Clinic. There was no obvious defect in the eyes, ears and kidneys of Eya3 mutant mice. Homozygous mutants displayed decreased bone mineral content and shorter body length. In the lung, the tidal volume at rest was decreased, and electrocardiography showed increased JT- and PQ intervals as well as decreased QRS amplitude. Behavioral analysis of the mutants demonstrated a mild increase in exploratory behavior, but decreased locomotor activity and reduced muscle strength. Analysis of differential gene expression revealed 110 regulated genes in heart and brain. Using real-time PCR, we confirmed Nup155 being down regulated in both organs.

conclusionThe loss of Eya3 in the mouse has no apparent effect on eye development. The wide-spread expression of Eya3 in mouse and zebrafish embryos is in contrast to the restricted expression pattern in Xenopus embryos. The loss of Eya3 in mice leads to a broad spectrum of minor physiological changes. Among them, the mutant mice move less than the wild-type mice and, together with the effects on respiratory, muscle and heart function, the mutation might lead to more severe effects when the mice become older. Therefore, future investigations of Eya3 function should focus on aging mice.

Indexed as

AnimalsBase SequenceDNADNA-Binding ProteinsEyeFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalHomozygoteIn Situ HybridizationLac OperonMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicDNADNA-Binding ProteinsEya3 protein, mouseZebrafish Proteins

Identifiers

PMID19102749
PMCPMC2653502
OpenAlexW2000115036

What OpenQuestion holds

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LicenceCC BY
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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.