The striking conservation between genes involved in cytokinesis and axonal elongation, as well as the morphological similarity between growth cones and migrating cells, raises the question of how axonal elongation evolved. Based on the observation that axonal elongation, like cell migration, involves retrograde actin flow at the leading edge and bulk forward advance of microtubules, we have developed and applied an active fluid biophysical model to cell division, mesenchymal cell migration, ameboid migration, neuronal migration, and axonal elongation. We find patterns of motion can be simulated in all cases by modestly adjusting sub-cellular gradients in cellular adhesion, force generation, cytoskeletal viscosity, and cellular topology. Considering this problem in an evolutionary context suggests a hypothetical path linking them together, a means for testing whether neurons evolved once or twice during evolution, and new directions for developing therapies designed to treat neurological injury and disease.
Learning Objectives:
1. Classify the core mechanism underlying cell motility and how to interpret kymographs.
2. Identify the differences and commonalities between the internal flow patterns and motion that occur during cytokinesis, amoeboid migration, mesenchymal migration, neuronal migration, and axonal elongation.
3. Approve that cell biological and biophysical analysis of axonal elongation may help us to better understand how neurons evolved.