DIP-2 suppresses ectopic neurite sprouting and axonal regeneration in mature neurons release_pl6oyans5bfmlopnyspohf3b7e

by Nathaniel Noblett, Zilu Wu, Zhao Hua Ding, Seungmee Park, Tony Roenspies, Stephane Flibotte, Andrew Chisholm, Yishi Jin, Antonio Colavita

Published in Journal of Cell Biology by Rockefeller University Press.

2018   Volume 218, p125-133


Neuronal morphology and circuitry established during early development must often be maintained over the entirety of animal lifespans. Compared with neuronal development, the mechanisms that maintain mature neuronal structures and architecture are little understood. The conserved disco-interacting protein 2 (DIP2) consists of a DMAP1-binding domain and two adenylate-forming domains (AFDs). We show that the <jats:italic>Caenorhabditis elegans</jats:italic> DIP-2 maintains morphology of mature neurons. <jats:italic>dip-2</jats:italic> loss-of-function mutants display a progressive increase in ectopic neurite sprouting and branching during late larval and adult life. In adults, <jats:italic>dip-2</jats:italic> also inhibits initial stages of axon regeneration cell autonomously and acts in parallel to DLK-1 MAP kinase and EFA-6 pathways. The function of DIP-2 in maintenance of neuron morphology and in axon regrowth requires its AFD domains and is independent of its DMAP1-binding domain. Our findings reveal a new conserved regulator of neuronal morphology maintenance and axon regrowth after injury.
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