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Elife. 2017 Jan 18;6. pii: e20172. doi: 10.7554/eLife.20172.

Genetic defects in β-spectrin and tau sensitize C. elegans axons to movement-induced damage via torque-tension coupling.

Author information

1
Department of Molecular and Cellular Physiology, Stanford University, Stanford, United States.
2
Department of Chemical Engineering, Stanford University, Stanford, United States.
3
Department of Informatics, Technical University of Munich, , Germany.
4
Department of Biology, Stanford University, Stanford, United States.

Abstract

Our bodies are in constant motion and so are the neurons that invade each tissue. Motion-induced neuron deformation and damage are associated with several neurodegenerative conditions. Here, we investigated the question of how the neuronal cytoskeleton protects axons and dendrites from mechanical stress, exploiting mutations in UNC-70 β-spectrin, PTL-1 tau/MAP2-like and MEC-7 β-tubulin proteins in Caenorhabditis elegans. We found that mechanical stress induces supercoils and plectonemes in the sensory axons of spectrin and tau double mutants. Biophysical measurements, super-resolution, and electron microscopy, as well as numerical simulations of neurons as discrete, elastic rods provide evidence that a balance of torque, tension, and elasticity stabilizes neurons against mechanical deformation. We conclude that the spectrin and microtubule cytoskeletons work in combination to protect axons and dendrites from mechanical stress and propose that defects in β-spectrin and tau may sensitize neurons to damage.

KEYWORDS:

C. elegans; STED microscopy; axonal mechanics; cell biology; confocal microscopy; cytoskeleton; discrete elastic rods; electron microscopy; neuroscience

PMID:
28098556
PMCID:
PMC5298879
DOI:
10.7554/eLife.20172
[Indexed for MEDLINE]
Free PMC Article

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