Evidence map›Paper›PMID 18971454›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Formin-dependent synaptic growth: evidence that Dlar signals via Diaphanous to modulate synaptic actin and dynamic pioneer microtubules.

Catherine Pawson, Benjamin A Eaton, Graeme W Davis

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  6. Article
  7. The synaptic life of microtubules.Current opinion in neurobiology · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Dynamic microtubules at the synapse.Current opinion in neurobiology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. A Screen for Synaptic Growth Mutants Reveals Mechanisms That Stabilize Synaptic Strength.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Article
  19. 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

3 authors at 2 institutions in 2 countries.

Catherine PawsonDepartment of Biochemistry and Biophysics, Programs in Neuroscience and Cell Biology, University of California, San Francisco, San Francisco, California 94158-2822, USA.
Benjamin A Eaton
Graeme W Davis
Laboratoire d’immunologie intégrative du cancer · FRUniversity of California, San Francisco · US

Funding

Molecular and Cellular Mechanisms of Synaptic GrowthR01NS047342 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2004 to 2012
$3.0M
Molecular and Cellular Mechanisms of Synaptic GrowthR37NS047342 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAVIS, GRAEME W · 2013 to 2016
$1.4M
NINDS NIH HHS NS047342NINDS NIH HHS R01 NS047342NINDS NIH HHS R37 NS047342
6 · The paper itself

Abstract

The diaphanous gene is the founding member of a family of Diaphanous-related formin proteins (DRFs). We identified diaphanous in a screen for genes that are necessary for the normal growth and stabilization of the Drosophila neuromuscular junction (NMJ). Here, we demonstrate that diaphanous mutations perturb synaptic growth at the NMJ. Diaphanous protein is present both presynaptically and postsynaptically. However, genetic rescue experiments in combination with additional genetic interaction experiments support the conclusion that dia is necessary presynaptically for normal NMJ growth. We then document defects in both the actin and microtubule cytoskeletons in dia mutant nerve terminals. In so doing, we define and characterize a population of dynamic pioneer microtubules within the NMJ that are distinct from the bundled core of microtubules identified by the MAP1b-like protein Futsch. Defects in both synaptic actin and dynamic pioneer microtubules are correlated with impaired synaptic growth in dia mutants. Finally, we present genetic evidence that Dia functions downstream of the presynaptic receptor tyrosine phosphatase Dlar and the Rho-type GEF (guanine nucleotide exchange factor) trio to control NMJ growth. Based on the established function of DRFs as Rho-GTPase-dependent regulators of the cell cytoskeleton, we propose a model in which Diaphanous links receptor tyrosine phosphatase signaling at the plasma membrane to growth-dependent modulation of the synaptic actin and microtubule cytoskeletons.

Indexed as

ActinsAnimalsAnimals, Genetically ModifiedCarrier ProteinsCells, CulturedDrosophilaDrosophila ProteinsFetal ProteinsForminsMicrofilament ProteinsMicrotubulesNerve Tissue ProteinsNeuromuscular JunctionNuclear ProteinsReceptor-Like Protein Tyrosine PhosphatasesSignal TransductionActinsCarrier Proteinsdiaphanous protein, DrosophilaDrosophila ProteinsFetal ProteinsForminsLar protein, DrosophilaMicrofilament ProteinsNerve Tissue ProteinsNuclear ProteinsReceptor-Like Protein Tyrosine Phosphatases

Identifiers

PMID18971454
PMCPMC2654187
OpenAlexW1992810376

What OpenQuestion holds

Textmetadata
LicenceTDM
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.