The microtubule-severing protein fidgetin acts after dendrite injury to promote their degeneration

Juan Tao, Chengye Feng, Melissa M. Rolls

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

After being severed from the cell body, axons initiate an active degeneration program known as Wallerian degeneration. Although 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 used a Drosophila model to identify microtubule regulators involved in dendrite degeneration. We found that, when levels of fidgetin were reduced using mutant or RNA interference (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 tomoderate microtubule stability in dendrites, or (2) by acting specifically after injury to disassemble microtubules. When comparing microtubule dynamics and stability in uninjured neurons with and 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 microtubules in dendrites severed from the cell body.

Original languageEnglish (US)
Pages (from-to)3274-3281
Number of pages8
JournalJournal of Cell Science
Volume129
Issue number17
DOIs
StatePublished - Jan 1 2016

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Microtubule Proteins
Dendrites
Microtubules
Wounds and Injuries
Neuronal Plasticity
Wallerian Degeneration
RNA Interference
Drosophila
Axons
Neurons

All Science Journal Classification (ASJC) codes

  • Cell Biology

Cite this

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abstract = "After being severed from the cell body, axons initiate an active degeneration program known as Wallerian degeneration. Although 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 used a Drosophila model to identify microtubule regulators involved in dendrite degeneration. We found that, when levels of fidgetin were reduced using mutant or RNA interference (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 tomoderate microtubule stability in dendrites, or (2) by acting specifically after injury to disassemble microtubules. When comparing microtubule dynamics and stability in uninjured neurons with and 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 microtubules in dendrites severed from the cell body.",
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The microtubule-severing protein fidgetin acts after dendrite injury to promote their degeneration. / Tao, Juan; Feng, Chengye; Rolls, Melissa M.

In: Journal of Cell Science, Vol. 129, No. 17, 01.01.2016, p. 3274-3281.

Research output: Contribution to journalArticle

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