Abstract
ABSTRACTThe microtubule-based molecular motor dynein is essential for proper neuronal morphogenesis. Dynein activity is regulated by cofactors, and the role(s) of these cofactors in shaping neuronal structure are still being elucidated. Using Drosophila melanogaster, we reveal that the loss of the dynein cofactor NudE results in abnormal dendrite arborization. Our data show that NudE associates with Golgi outposts, which mediate dendrite branching, suggesting that NudE normally influences dendrite patterning by regulating Golgi outpost transport. Neurons lacking NudE also have increased microtubule dynamics, reflecting a change in microtubule stability that is likely to also contribute to abnormal dendrite growth and branching. These defects in dendritogenesis are rescued by elevating levels of Lis1, another dynein cofactor that interacts with NudE as part of a tripartite complex. Our data further show that the NudE C-terminus is dispensable for dendrite morphogenesis and is likely to modulate NudE activity. We propose that a key function of NudE is to enhance an interaction between Lis1 and dynein that is crucial for motor activity and dendrite architecture.
Highlights
Neuronal morphology is integral to neuronal function, affecting both the inputs that a neuron receives and the pattern of connectivity
The dynein cofactor nuclear distribution E (NudE) is necessary for neuronal morphogenesis To determine whether the loss of NudE disrupts axon and/or dendrite morphogenesis, we utilized the class IV da neurons in Drosophila as a model
Control axons emerged from the ddaC cell bodies as a single process that extended unbranched into the ventral nerve cord, whereas the axons projected by neurons lacking NudE formed multiple fine branches a short distance from the soma (Fig. 1B,C)
Summary
Neuronal morphology is integral to neuronal function, affecting both the inputs that a neuron receives and the pattern of connectivity. In addition to mediating the transport of diverse cargo, dynein and kinesin have been shown to regulate the orientation of microtubules in axons and dendrites (Kapitein and Hoogenraad, 2011; Kapitein et al, 2010; Lin et al, 2012; Yan et al, 2013; Zheng et al, 2008). It remains largely unknown how motor function is regulated to carry out different activities within a single neuron.
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