Neuronal polarization is impaired in mice lacking RhoE expression
Article first published online: 13 APR 2012
© 2012 The Authors. Journal of Neurochemistry © 2012 International Society for Neurochemistry
Journal of Neurochemistry
Volume 121, Issue 6, pages 903–914, June 2012
How to Cite
Peris, B., Gonzalez-Granero, S., Ballester-Lurbe, B., García-Verdugo, J.-M., Pérez-Roger, I., Guerri, C., Terrado, J. and Guasch, R. M. (2012), Neuronal polarization is impaired in mice lacking RhoE expression. Journal of Neurochemistry, 121: 903–914. doi: 10.1111/j.1471-4159.2012.07733.x
- Issue published online: 8 JUN 2012
- Article first published online: 13 APR 2012
- Accepted manuscript online: 16 MAR 2012 03:18PM EST
- Received August 2, 2011; revised manuscript received March 13, 2012; accepted March 13, 2012.
- neuronal polarization;
J. Neurochem. (2012) 121, 903–914.
Proper development of neuronal networks relies on the polarization of the neurons, thus the establishment of two compartments, axons and dendrites, whose formation depends on cytoskeletal rearrangements. Rnd proteins are regulators of actin organization and they are important players in several aspects of brain development as neurite formation, axon guidance and neuron migration. We have recently demonstrated that mice lacking RhoE/Rnd3 expression die shortly after birth and have neuromotor impairment and neuromuscular alterations, indicating an abnormal development of the nervous system. In this study, we have further investigated the specific role played by RhoE in several aspects of neuronal development by using hippocampal neuron cultures. Our findings show that neurons from a mice lacking RhoE expression exhibit a decrease in the number and the total length of the neurites. We also show that RhoE-deficient neurons display a reduction in axon outgrowth and a delay in the process of neuronal polarization. In addition, our results suggest an involvement of the RHOA/ROCK/LIMK/COFILIN signaling pathway in the neuronal alterations induced by the lack of RhoE. These findings support our previous report revealing the important role of RhoE in the normal development of the nervous system and may provide novel therapeutic targets in neurodegenerative disorders.