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Loss of MEC-17 leads to microtubule instability and axonal degeneration.

Authors
  • Neumann, Brent
  • Hilliard, Massimo A
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Jan 16, 2014
Volume
6
Issue
1
Pages
93–103
Identifiers
DOI: 10.1016/j.celrep.2013.12.004
PMID: 24373971
Source
Medline
License
Unknown

Abstract

Axonal degeneration arises as a consequence of neuronal injury and is a common hallmark of a number of neurodegenerative diseases. However, the genetic causes and the cellular mechanisms that trigger this process are still largely unknown. Based on forward genetic screening in C. elegans, we have identified the α-tubulin acetyltransferase gene mec-17 as causing spontaneous, adult-onset, and progressive axonal degeneration. Loss of MEC-17 leads to microtubule instability, a reduction in mitochondrial number, and disrupted axonal transport, with altered distribution of both mitochondria and synaptic components. Furthermore, mec-17-mediated axonal degeneration occurs independently from its acetyltransferase domain; is enhanced by mutation of coel-1, a tubulin-associated molecule; and correlates with the animal's body length. This study therefore identifies a critical role for the conserved microtubule-associated protein MEC-17 in preserving axon integrity and preventing axonal degeneration.

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