Loss of Maspardin Attenuates Growth of Mouse Neurons
Document Type
Thesis
Degree Name
Master of Science (MS)
Department
Biological and Environmental Sciences
Date of Award
Spring 2014
Abstract
Mast syndrome is an autosomal-recessive, progressive form of hereditary spastic paraplegia (HSP), caused by a mutation in ACP33/maspardin gene. However, molecular function of maspardin remains unclear. Based on the preferential expression of maspardin in motor neurons, we hypothesized that maspardin regulates the growth of cortical neurons. To test this hypothesis, cortical neurons were isolated from wild type (ACP33+/+) and knockout (ACP33-/-) mice and their growth was compared in vitro. Relative to ACP33+/+, there was 3.6x reduction in the growth of ACP33-/- neurons at 96 hr (p<0.05). While the addition of EGF growth factor further increased the growth of ACP33+/+ neurons at 96 hr (2x, p<0.05), it had no effect in ACP33-/- neuronal growth. In summary, our results suggest that maspardin is indispensable for the growth and differentiation of cortical neurons. Deciphering molecular mechanisms of maspardin mediated motor neuronal growth may lead to strategies for reversing spastic paraplegia in mast syndrome patients.
Advisor
Venugopalan Cheriyath
Subject Categories
Biochemistry, Biophysics, and Structural Biology | Life Sciences
Recommended Citation
Davenport, Anne Mignon, "Loss of Maspardin Attenuates Growth of Mouse Neurons" (2014). Electronic Theses & Dissertations. 571.
https://digitalcommons.tamuc.edu/etd/571
