After being severed from the cell body, axons initiate an active degeneration program known as Wallerian degeneration. While dendrites also seem to have an active injury-induced degeneration program, no endogenous regulators of this process are known. Because microtubule disassembly has been proposed to play a role in both pruning and injury-induced degeneration, we tested microtubule regulators to determine whether any of them were involved in dendrite degeneration. We found that, when levels of fidgetin were reduced using mutant or RNAi strategies, dendrite degeneration was delayed, but axon degeneration and dendrite pruning proceeded with normal timing. We explored two possible ways in which fidgetin could promote dendrite degeneration: 1) by acting constitutively to moderate microtubule stability in dendrites, or 2) by acting specifically after injury to disassemble microtubules. By comparing microtubule dynamics and stability in uninjured neurons without fidgetin we could not find evidence that fidgetin regulated microtubule stability constitutively. However, we identified a fidgetin-dependent increase in microtubule dynamics in severed dendrites. We conclude that fidgetin acts after injury to promote disassembly of dendrites severed from the cell body.
- Received February 25, 2016.
- Accepted July 8, 2016.
- © 2016. Published by The Company of Biologists Ltd