Most contemporary studies have speculated that bouts of elongation involve polymerization of the cytoskeleton whereas bouts of retraction involve depolymerization of the cytoskeleton. Here we present an alternative view, namely that molecular motor proteins generate forces on the cytoskeletal polymers that can affect their distribution and configuration. In this view, bouts of axonal elongation involve net forward movement of cytoskeletal elements whereas bouts of retraction involve net backward movements. We propose that environmental cues elicit bouts of elongation or retraction via biochemical pathways that modulate the activities of relevant motors. Ahmad, F.J., J. Hughey, T. Wittmann, A. Hyman, M. Greaser, and P.W. Baas.
Motor proteins regulate force interactions between microtubules and microfilaments in the axon.
In this article, we test the hypothesis that motor-driven forces integrate the microtubule and microfilament systems of the axon. It has long been known that microtubule depletion causes axons to retract in a microfilament-dependent manner. Here we show that axon retraction occurs when cytoplasmic dynein is disabled, even though the microtubules are left intact. This retraction can be rescued if myosins are disabled, even though the microfilaments are left intact. Yu, W., C. Cook, C. Sauter, R. Kuriyama, P.L. Kaplan, and P.W. Baas.