Evidence map›Paper›PMID 15157419›Full record

ArticleNeuron2004

New synaptic bouton formation is disrupted by misregulation of microtubule stability in aPKC mutants.

Catalina Ruiz-Canada, James Ashley, Stephanie Moeckel-Cole, Eric Drier, Jerry Yin, Vivian Budnik

Abstract read
In one paragraph

Article in Neuron, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
–field-weighted citation impact
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

84 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. The synaptic life of microtubules.Current opinion in neurobiology · 2021
    Review
  15. Changes in Presynaptic Gene Expression during Homeostatic Compensation at a Central Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. Article
  17. Article
  18. Dynamic microtubules at the synapse.Current opinion in neurobiology · 2020
    Review
  19. Article
  20. Article

24 more citing papers are in PubMed but not listed here.

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.

Catalina Ruiz-CanadaDepartment of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605 USA.
James Ashley
Stephanie Moeckel-Cole
Eric Drier
Jerry Yin
Vivian Budnik

Funding

MORPHOLOGICAL PLASTICITY AT THE NEUROMUSCULAR JUNCTIONR01NS030072 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BUDNIK, VIVIAN G. · 1992 to 2009
$2.7M
Spatial- Temporal Aspects of Drosophila Memory FormationR01MH067774 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI YIN, JERRY C · 2003 to 2007
$1.7M
Circadian Influences in Drosophila Memory FormationR21DA015753 · NIDA · COLD SPRING HARBOR LABORATORY · PI YIN, JERRY C · 2002 to 2003
$332k
NIMH NIH HHS R01 MH067774NINDS NIH HHS R01 NS030072NINDS NIH HHS R01 NS3700
6 · The paper itself

Abstract

The Baz/Par-3-Par-6-aPKC complex is an evolutionarily conserved cassette critical for the development of polarity in epithelial cells, neuroblasts, and oocytes. aPKC is also implicated in long-term synaptic plasticity in mammals and the persistence of memory in flies, suggesting a synaptic function for this cassette. Here we show that at Drosophila glutamatergic synapses, aPKC controls the formation and structure of synapses by regulating microtubule (MT) dynamics. At the presynapse, aPKC regulates the stability of MTs by promoting the association of the MAP1Brelated protein Futsch to MTs. At the postsynapse, aPKC regulates the synaptic cytoskeleton by controlling the extent of Actin-rich and MT-rich areas. In addition, we show that Baz and Par-6 are also expressed at synapses and that their synaptic localization depends on aPKC activity. Our findings establish a novel role for this complex during synapse development and provide a cellular context for understanding the role of aPKC in synaptic plasticity and memory.

Indexed as

Intracellular Signaling Peptides and ProteinsActin CytoskeletonAnimalsCaenorhabditis elegans ProteinsCarrier ProteinsCell DifferentiationDrosophila melanogasterDrosophila ProteinsGlutamic AcidMemoryMicrotubule-Associated ProteinsMicrotubulesMutationNerve Growth FactorsNervous SystemNeuronal Plasticitybaz protein, DrosophilaCaenorhabditis elegans ProteinsCarrier ProteinsDrosophila Proteinsfutsch protein, DrosophilaGlutamic AcidIntracellular Signaling Peptides and ProteinsMicrotubule-Associated ProteinsNerve Growth FactorsPAR-3 protein, C eleganspar-6 protein, C elegansPKC-3 proteinProtein Kinase CProteinsProtein Serine-Threonine Kinases

Identifiers

PMID15157419
PMCPMC4656022

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.