Evidence map›Paper›PMID 26976084›Full record

ArticleScientific reports2016

Deletion of endogenous Tau proteins is not detrimental in Drosophila.

Sylvie Burnouf, Sebastian Grönke, Hrvoje Augustin, Jacqueline Dols, Marianna Karina Gorsky, Jennifer Werner, Fiona Kerr, Nazif Alic, Pedro Martinez, Linda Partridge

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

39 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Tau protein as a regulator of mitochondrial function and dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. GSK-3β coordinates axonal microtubule organization through Shot and Tau.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Tau Regulates Endoreplication inmicroPublication biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. TBI and Tau Loss of Function Both Affect Naïve Ethanol Sensitivity inInternational journal of molecular sciences · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. The Effect of theInternational journal of molecular sciences · 2023
    Article
  17. Frontiers in neuroscience · 2023
    Review
  18. Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023
    Review
  19. Journal of biosciences · 2023
    Review
  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

10 authors at 3 institutions in 2 countries.

Sylvie BurnoufMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Sebastian GrönkeMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Hrvoje AugustinInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London, WC1E 6BT, UK.
Jacqueline DolsMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Marianna Karina GorskyMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Jennifer WernerMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Fiona KerrInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London, WC1E 6BT, UK.
Nazif AlicInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London, WC1E 6BT, UK.
Pedro MartinezInstitute of Healthy Ageing, Department of Genetics, Evolution and Environment, University College London, Darwin Building, Gower Street, London, WC1E 6BT, UK.
Linda PartridgeMax Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity College London · GBMax Planck Institute for Biology of Ageing · DE

Funding

Biotechnology and Biological Sciences Research Council BB/M029093/1
6 · The paper itself

Abstract

Human Tau (hTau) is a highly soluble and natively unfolded protein that binds to microtubules within neurons. Its dysfunction and aggregation into insoluble paired helical filaments is involved in the pathogenesis of Alzheimer's disease (AD), constituting, together with accumulated β-amyloid (Aβ) peptides, a hallmark of the disease. Deciphering both the loss-of-function and toxic gain-of-function of hTau proteins is crucial to further understand the mechanisms leading to neurodegeneration in AD. As the fruit fly Drosophila melanogaster expresses Tau proteins (dTau) that are homologous to hTau, we aimed to better comprehend dTau functions by generating a specific tau knock-out (KO) fly line using homologous recombination. We observed that the specific removal of endogenous dTau proteins did not lead to overt, macroscopic phenotypes in flies. Indeed, survival, climbing ability and neuronal function were unchanged in tau KO flies. In addition, we did not find any overt positive or negative effect of dTau removal on human Aβ-induced toxicity. Altogether, our results indicate that the absence of dTau proteins has no major functional impact on flies, and suggests that our tau KO strain is a relevant model to further investigate the role of dTau proteins in vivo, thereby giving additional insights into hTau functions.

Indexed as

Amyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedDrosophila melanogasterDrosophila ProteinsGene Knockdown TechniquesLife ExpectancyLocomotionNeuronstau ProteinsAmyloid beta-PeptidesDrosophila Proteinstau Proteins

Identifiers

PMID26976084
PMCPMC4792132
OpenAlexW2408449484

What OpenQuestion holds

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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.