| First Author | Cheever TR | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 3 | Pages | e17768 |
| PubMed ID | 21445349 | Mgi Jnum | J:171672 |
| Mgi Id | MGI:4950778 | Doi | 10.1371/journal.pone.0017768 |
| Citation | Cheever TR, et al. (2011) Axonal regeneration and neuronal function are preserved in motor neurons lacking ss-actin in vivo. PLoS One 6(3):e17768 |
| abstractText | The proper localization of ss-actin mRNA and protein is essential for growth cone guidance and axon elongation in cultured neurons. In addition, decreased levels of ss-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 ss-actin loss-of-function at growth cones or pre-synaptic nerve terminals could contribute to the pathogenesis of this disease. However, the role of ss-actin in motor neurons in vivo and its potential relevance to disease has yet to be examined. We therefore generated motor neuron specific ss-actin knock-out mice (Actb-MNsKO) to investigate the function of ss-actin in motor neurons in vivo. Surprisingly, ss-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 ss-actin is not required for motor neuron function or regeneration in vivo. |
