Genetic defects in β-spectrin and tau sensitize C. Elegans axons to movement-induced damage via torque-tension coupling
Krieg M, Stuehmer J, Cueva JG, Fetter R, Spilker K, Cremers D, Shen K, Dunn AR, Goodman MB (2017)
Publication Type: Journal article
Publication year: 2017
Journal
Book Volume: 6
Article Number: e20172
DOI: 10.7554/eLife.20172
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.
Involved external institutions
United States (USA) (US)
Germany (DE)How to cite
APA:
Krieg, M., Stuehmer, J., Cueva, J.G., Fetter, R., Spilker, K., Cremers, D.,... Goodman, M.B. (2017). Genetic defects in β-spectrin and tau sensitize C. Elegans axons to movement-induced damage via torque-tension coupling. eLife, 6. https://doi.org/10.7554/eLife.20172
MLA:
Krieg, Michael, et al. "Genetic defects in β-spectrin and tau sensitize C. Elegans axons to movement-induced damage via torque-tension coupling." eLife 6 (2017).
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