Axonal Regeneration and Neuronal Function Are Preserved in Motor Neurons Lacking β-Actin In Vivo

In The proper localization of beta-actin mRNA and protein is essential for growth cone guidance and axon elongation in cultured neurons. In addition, decreased levels of beta-actin mRNA and protein have been identified in the growth cones of motor neurons cultured from a mouse model of Spinal Muscular Atrophy (SMA), suggesting that beta-actin loss-of-function at growth cones or pre-synaptic nerve terminals could contribute to the pathogenesis of this disease. However, the role of beta-actin in motor neurons in vivo and its potential relevance to disease has yet to be examined. We therefore generated motor neuron specific beta-actin knock-out mice (Actb-MNsKO) to investigate the function of beta-actin in motor neurons in vivo. Surprisingly, beta-actin was not required for motor neuron viability or neuromuscular junction maintenance. Skeletal muscle from Actb-MNsKO mice showed no histological indication of denervation and did not significantly differ from controls in several measurements of physiologic function. Finally, motor axon regeneration was unimpaired in Actb-MNsKO mice, suggesting that beta-actin is not required for motor neuron function or regeneration in vivo.