Evidence map›Paper›PMID 27705774›Full record

ArticleBiophysical journal2016

Mechanism of Axonal Contractility in Embryonic Drosophila Motor Neurons In Vivo.

Alireza Tofangchi, Anthony Fan, M Taher A Saif

Abstract read
In one paragraph

Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Tension shapes memory: computational insights into neural plasticity.Frontiers in computational neuroscience · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The role of mechanics in axonal stability and development.Seminars in cell & developmental biology · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Axonal cytomechanics in neuronal development.Journal of biosciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Physical Biology of Axonal Damage.Frontiers in cellular neuroscience · 2018
    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

3 authors.

Alireza TofangchiDepartment of Mechanical Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois.
Anthony FanDepartment of Mechanical Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois.
M Taher A SaifDepartment of Mechanical Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois. Electronic address: saif@illinois.edu.

Funding

Mechanical Force and Neural RegenerationR01NS063405 · NINDS · UNIVERSITY OF MIAMI CORAL GABLES · PI CHIBA, AKIRA, JAKOBSSON, ERIC G · 2008 to 2011
$1.2M
NINDS NIH HHS R01 NS063405
6 · The paper itself

Abstract

Several in vitro and limited in vivo experiments have shown that neurons maintain a rest tension along their axons intrinsically. They grow in response to stretch but contract in response to loss of tension. This contraction eventually leads to the restoration of the rest tension in axons. However, the mechanism by which axons maintain tension in vivo remains elusive. The objective of this work is to elucidate the key cytoskeletal components responsible for generating tension in axons. Toward this goal, in vivo experiments were conducted on single axons of embryonic Drosophila motor neurons in the presence of various drugs. Each axon was slackened mechanically by bringing the neuromuscular junction toward the central nervous system multiple times. In the absence of any drug, axons shortened and restored the straight configuration within 2-4 min of slackening. The total shortening was ∼40% of the original length. The recovery rate in each cycle, but not the recovery magnitude, was dependent on the axon's prior contraction history. For example, the contraction time of a previously slackened axon may be twice its first-time contraction. This recovery was significantly hampered with the depletion of ATP, inhibition of myosin motors, and disruption of actin filaments. The disruption of microtubules did not affect the recovery magnitude, but, on the contrary, led to an enhanced recovery rate compared to control cases. These results suggest that the actomyosin machinery is the major active element in axonal contraction, whereas microtubules contribute as resistive/dissipative elements.

Indexed as

ActinsAdenosine TriphosphateAnimalsAnimals, Genetically ModifiedAxonsCells, CulturedCell SizeDrosophilaDrosophila ProteinsGreen Fluorescent ProteinsMotor NeuronsMyosin-Light-Chain KinaseMyosin Type IINeuronal Outgrowthrho-Associated KinasesSurface PropertiesActinsAdenosine TriphosphateDrosophila ProteinsGreen Fluorescent ProteinsMyosin-Light-Chain KinaseMyosin Type IIrho-Associated Kinases

Identifiers

PMID27705774
PMCPMC5052456

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.