Evidence map›Paper›PMID 10908619›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Depletion of a microtubule-associated motor protein induces the loss of dendritic identity.

W Yu, C Cook, C Sauter, R Kuriyama, P L Kaplan, P W Baas

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

52 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Kinetochore proteins control microtubule dynamics in postmitotic neurons to regulate the formation of dendritic spines.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. An in vitro model of neuronal ensembles.Nature communications · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Microtubule Dysfunction: A Common Feature of Neurodegenerative Diseases.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Polarity Sorting of Microtubules in the Axon.Trends in neurosciences · 2018
    Review
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 1 country.

W YuDepartment of Anatomy, The University of Wisconsin Medical School, Madison 53706, USA.
C Cook
C Sauter
R Kuriyama
P L Kaplan
P W Baas
University of Wisconsin–Madison · USUniversity of Minnesota Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendrites are short stout tapering processes that are rich in ribosomes and Golgi elements, whereas axons are long thin processes of uniform diameter that are deficient in these organelles. It has been hypothesized that the unique morphological and compositional features of axons and dendrites result from their distinct patterns of microtubule polarity orientation. The microtubules within axons are uniformly oriented with their plus ends distal to the cell body, whereas microtubules within dendrites are nonuniformly oriented. The minus-end-distal microtubules are thought to arise via their specific transport into dendrites by the motor protein known as CHO1/MKLP1. According to this model, CHO1/MKLP1 transports microtubules with their minus ends leading into dendrites by generating forces against the plus-end-distal microtubules, thus creating drag on the plus-end-distal microtubules. Here we show that depletion of CHO1/MKLP1 from cultured neurons causes a rapid redistribution of microtubules within dendrites such that minus-end-distal microtubules are chased back to the cell body while plus-end-distal microtubules are redistributed forward. The dendrite grows significantly longer and thinner, loses its taper, and acquires a progressively more axon-like organelle composition. These results suggest that the forces generated by CHO1/MKLP1 are necessary for maintaining the minus-end-distal microtubules in the dendrite, for antagonizing the anterograde transport of the plus-end-distal microtubules, and for sustaining a pattern of microtubule organization necessary for the maintenance of dendritic morphology and composition. Thus, we would conclude that dendritic identity is dependent on forces generated by CHO1/MKLP1.

Indexed as

AnimalsAxonsCells, CulturedCell SizeDendritesFluorescent DyesIsoquinolinesMicroscopy, ElectronMicrotubule-Associated ProteinsMicrotubulesMolecular Motor ProteinsNeurofilament ProteinsNeuronsOligonucleotides, AntisenseRatsSuperior Cervical GanglionFluorescent DyesIsoquinolineslucifer yellowMicrotubule-Associated ProteinsMolecular Motor ProteinsNeurofilament ProteinsOligonucleotides, Antisense

Identifiers

PMID10908619
PMCPMC6772545
OpenAlexW1583142746

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.