Abstract
The Golgi apparatus is a dynamic organelle involved in processing and sorting of lipids and proteins. In neurons, the Golgi apparatus is important for the development of axons and dendrites and maintenance of their highly complex polarized morphology. The motor protein complex cytoplasmic dynein has an important role in Golgi apparatus positioning and function. Together, with dynactin and other regulatory factors it drives microtubule minus-end directed motility of Golgi membranes. Inhibition of dynein results in fragmentation and dispersion of the Golgi ribbon in the neuronal cell body, resembling the Golgi abnormalities observed in some neurodegenerative disorders, in particular motor neuron diseases. Mutations in dynein and its regulatory factors, including the dynactin subunit p150Glued, BICD2 and Lis-1, are associated with several human nervous system disorders, including cortical malformation and motor neuropathy. Here we review the role of dynein and its regulatory factors in Golgi function and positioning, and the potential role of dynein malfunction in causing Golgi apparatus abnormalities in nervous system disorders.
Highlights
The Golgi apparatus consists of stacks of biochemically and functionally heterogeneous diskshaped cisternae
The biogenesis and maintenance of the Golgi ribbon structure and position strongly depends on the microtubule cytoskeleton and microtubule motors, in particular cytoplasmic dynein that drives microtubule minus-end transport
P150glued interacts with Sec23 of the COPII vesicle coat complex that sort cargo into budding vesicles at endoplasmic reticulum (ER) exit sites for their delivery at the juxtaposed tubulo-vesicular ER-Golgi intermediate compartment (ERGIC)
Summary
The Golgi apparatus consists of stacks of biochemically and functionally heterogeneous diskshaped cisternae. The Golgi stacks are laterally connected to form a single continuous membrane system, termed the Golgi ribbon that usually localizes near the centrosome (Klumperman, 2011). Golgi ribbon size and morphology may vary between cell types according to specific requirements of the secretory pathway (Yadav and Linstedt, 2011; Nakamura et al, 2012; Watanabe et al, 2014). Microtubule depolymerization with nocodazole results in the fragmentation of the Golgi ribbon, and the rebuilding of secretion competent ministacks dispersed throughout the cell at endoplasmic reticulum (ER) exit sites.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
