期刊
CELL REPORTS
卷 6, 期 1, 页码 93-103出版社
CELL PRESS
DOI: 10.1016/j.celrep.2013.12.004
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资金
- National Institutes of Health (NIH) National Center for Research Resources
- International C. elegans Gene Knockout Consortium
- NIH [R01NS060129]
- National Health and Medical Research Council [569500, 631634]
- Australian Research Council
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS060129] Funding Source: NIH RePORTER
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 alpha-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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