Evidence map›Paper›PMID 15772149›Full record

ArticleMolecular biology of the cell2005

Disruption of the MAP1B-related protein FUTSCH leads to changes in the neuronal cytoskeleton, axonal transport defects, and progressive neurodegeneration in Drosophila.

Alexandre Bettencourt da Cruz, Martin Schwärzel, Sabine Schulze, Mahtab Niyyati, Martin Heisenberg, Doris Kretzschmar

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

60 citing papers in PubMed, 89 citations in OpenAlex.

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  8. The Effect of theInternational journal of molecular sciences · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. The microtubule regulatorGenes & development · 2020
    Article
  13. Article
  14. Review
  15. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  16. Article
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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

6 authors at 2 institutions in 2 countries.

Alexandre Bettencourt da CruzCROET-Oregon Health and Science University, Portland, OR 97239, USA.
Martin Schwärzel
Sabine Schulze
Mahtab Niyyati
Martin Heisenberg
Doris Kretzschmar
Oregon Health & Science University · USUniversity of Würzburg · DE

Funding

SWS/NTE function in neurodegeneration and axonopathyR01NS047663 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI KRETZSCHMAR, DORIS · 2004 to 2013
$2.7M
NINDS NIH HHS R01 NS047663NINDS NIH HHS R01 NS047663-01
6 · The paper itself

Abstract

The elaboration of neuronal axons and dendrites is dependent on a functional cytoskeleton. Cytoskeletal components have been shown to play a major role in the maintenance of the nervous system through adulthood, and changes in neurofilaments and microtubule-associated proteins (MAPs) have been linked to a variety of neurodegenerative diseases. Here we show that Futsch, the fly homolog of MAP1B, is involved in progressive neurodegeneration. Although Futsch is widely expressed throughout the CNS, degeneration in futsch(olk) primarily occurs in the olfactory system and mushroom bodies. Consistent with the predicted function of Futsch, we find abnormalities in the microtubule network and defects in axonal transport. Degeneration in the adult brain is preceded by learning deficits, revealing a neuronal dysfunction before detectable levels of cell death. Futsch is negatively regulated by the Drosophila Fragile X mental retardation gene, and a mutation in this gene delays the onset of neurodegeneration in futsch(olk). A similar effect is obtained by expression of either fly or bovine tau, suggesting a certain degree of functional redundancy of MAPs. The futsch(olk) mutants exhibit several characteristics of human neurodegenerative diseases, providing an opportunity to study the role of MAPs in progressive neurodegeneration within an experimentally accessible, in vivo model system.

Indexed as

AnimalsAnimals, Genetically ModifiedAxonal TransportCattleCytoskeletonDrosophilaDrosophila ProteinsFemaleFragile X Messenger Ribonucleoprotein 1Genes, InsectMaleMicrotubule-Associated ProteinsMitochondriaMutationNerve DegenerationNerve Growth FactorsDrosophila ProteinsFMR1 protein, DrosophilaFragile X Messenger Ribonucleoprotein 1futsch protein, DrosophilaMicrotubule-Associated ProteinsNerve Growth FactorsRNA-Binding Proteinstau Proteins

Identifiers

PMID15772149
PMCPMC1087247
OpenAlexW2114099129

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.