Mechanism of Axonal Contractility in Embryonic Drosophila Motor Neurons in Vivo

Abstract

Several in vitro and limited in vivo experiments have shown that neurons maintain a rest tension along their axons intrinsically. They grow in response to stretch but contract in response to loss of tension. This contraction eventually leads to the restoration of the rest tension in axons. However, the mechanism by which axons maintain tension in vivo remains elusive. The objective of this work is to elucidate the key cytoskeletal components responsible for generating tension in axons. Towards this goal, in vivo experiments were conducted on single axons of embryonic drosophila motor neurons in the presence of various drugs. Each axon was slackened mechanically by bringing the neuromuscular junction (NMJ) towards the central nervous system (CNS) multiple times. In the absence of any drug, axons always shortened and restored the straight configuration each time within 2-4 minutes of slackening. The total shortening was about 40% of the original length. The recovery rate in each cycle, but not the recovery magnitude, was dependent on the number of times the axon had previously been slackened. This recovery was significantly hampered with the depletion of ATP, inhibition of myosin motors, and disruption of actin filaments, but not with the disruption of microtubules. These results suggest that the actomyosin-machinery is the major active element in axonal contraction while microtubules contribute passively as resistive elements.