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Modeling molecular mechanisms in the axon.

R de Rooij1, K E Miller2, E Kuhl1

  • 1Departments of Mechanical Engineering and Bioengineering, Stanford University, Stanford, CA 94305, USA.

Computational Mechanics
|June 13, 2017
PubMed
Summary

This study introduces a computational model explaining axon mechanical properties as emergent from molecular crosslinking. It reveals how crosslink density and dynamics influence stiffness, viscosity, and internal stress, driving axon elongation.

Keywords:
Finite elementactive forceaxonelasticityviscosity

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Area of Science:

  • Biophysics
  • Computational Biology
  • Cell Biology

Background:

  • Axons exhibit dynamic mechanical properties like stiffness and viscosity.
  • The molecular basis for these emergent cellular properties is not well understood.

Purpose of the Study:

  • To develop a computational mechanics model of axons.
  • To investigate how molecular-level events, specifically microtubule crosslinking, give rise to macroscopic axonal mechanical properties.
  • To explore the roles of passive and active crosslinking mechanisms in axon mechanics and elongation.

Main Methods:

  • Developed a discrete computational model of axons, representing microtubules and their crosslinking.
  • Simulated passive crosslinking (varying density and dynamics) and active crosslinking (involving dynein motors).
  • Analyzed the impact of crosslink density, detachment, and reattachment times on axonal stiffness, viscosity, and internal stress.

Main Results:

  • Axonal stiffness and viscosity increase linearly with crosslink density.
  • These mechanical properties are highly sensitive to the timing of crosslink detachment and reattachment.
  • Active crosslinking, utilizing dynein motors, was shown to generate internal stresses and actively drive axon elongation.

Conclusions:

  • The computational model successfully links molecular-level crosslinking to emergent cellular-level mechanical properties of axons.
  • Crosslink dynamics are critical determinants of axonal mechanical behavior.
  • Active crosslinking provides a mechanism for generating internal stress and driving axon growth, with implications for understanding both normal physiology and pathology.