Evidence map›Paper›PMID 22359556›Full record

ArticlePloS one2012

The role of actin turnover in retrograde actin network flow in neuronal growth cones.

David Van Goor, Callen Hyland, Andrew W Schaefer, Paul Forscher

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. 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
2.5field-weighted citation impact, top 11% 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, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. SiR-XActin: A Fluorescent Probe for Imaging Actin Dynamics in Live Cells.Angewandte Chemie (International ed. in English) · 2025
    Article
  4. Article
  5. Article
  6. Modeling the dynamics of actin and myosin during bleb stabilization.bioRxiv : the preprint server for biology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. An Integrated Cytoskeletal Model of Neurite Outgrowth.Frontiers in cellular neuroscience · 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

4 authors at 1 institution in 1 country.

David Van GoorDepartment of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut, United States of America.
Callen Hyland
Andrew W Schaefer
Paul Forscher
Yale University · US

Funding

Regulation of Neuronal Motility: the role of actin filament turnoverR01NS028695 · NINDS · YALE UNIVERSITY · PI FORSCHER, PAUL · 1990 to 2024
$7.8M
Ca and Rho GTPase Control of the Neuronal CytoskeletonR01NS051786 · NINDS · YALE UNIVERSITY · PI FORSCHER, PAUL · 2006 to 2009
$1.4M
NINDS NIH HHS R01 NS028695NINDS NIH HHS R01 NS051786NINDS NIH HHS R01-NS28695NINDS NIH HHS R01 NS51786
6 · The paper itself

Abstract

The balance of actin filament polymerization and depolymerization maintains a steady state network treadmill in neuronal growth cones essential for motility and guidance. Here we have investigated the connection between depolymerization and treadmilling dynamics. We show that polymerization-competent barbed ends are concentrated at the leading edge and depolymerization is distributed throughout the peripheral domain. We found a high-to-low G-actin gradient between peripheral and central domains. Inhibiting turnover with jasplakinolide collapsed this gradient and lowered leading edge barbed end density. Ultrastructural analysis showed dramatic reduction of leading edge actin filament density and filament accumulation in central regions. Live cell imaging revealed that the leading edge retracted even as retrograde actin flow rate decreased exponentially. Inhibition of myosin II activity before jasplakinolide treatment lowered baseline retrograde flow rates and prevented leading edge retraction. Myosin II activity preferentially affected filopodial bundle disassembly distinct from the global effects of jasplakinolide on network turnover. We propose that growth cone retraction following turnover inhibition resulted from the persistence of myosin II contractility even as leading edge assembly rates decreased. The buildup of actin filaments in central regions combined with monomer depletion and reduced polymerization from barbed ends suggests a mechanism for the observed exponential decay in actin retrograde flow. Our results show that growth cone motility is critically dependent on continuous disassembly of the peripheral actin network.

Indexed as

Actin CytoskeletonActinsAnimalsAntifungal AgentsCell MovementCells, CulturedDepsipeptidesGrowth ConesMyosin Type IINeuronsPolymerizationActinsAntifungal AgentsDepsipeptidesjasplakinolideMyosin Type II

Identifiers

PMID22359556
PMCPMC3281045
OpenAlexW2011530429

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.