TY - JOUR TI - Genetic defects in β-spectrin and tau sensitize C. elegans axons to movement-induced damage via torque-tension coupling AU - Krieg, Michael AU - Stühmer, Jan AU - Cueva, Juan G AU - Fetter, Richard AU - Spilker, Kerri AU - Cremers, Daniel AU - Shen, Kang AU - Dunn, Alexander R AU - Goodman, Miriam B A2 - Akhmanova, Anna VL - 6 PY - 2017 DA - 2017/01/18 SP - e20172 C1 - eLife 2017;6:e20172 DO - 10.7554/eLife.20172 UR - https://doi.org/10.7554/eLife.20172 AB - 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. KW - cytoskeleton KW - electron microscopy KW - confocal microscopy KW - STED microscopy KW - axonal mechanics KW - discrete elastic rods JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -