期刊
NATURE CELL BIOLOGY
卷 11, 期 8, 页码 1024-U263出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb1916
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资金
- National Institute of Neurological Diseases and Stroke
- Klingenstein Fellowship in the Neurosciences
- Irma T. Hirschl and Monique Weill-Caulier Trusts Career Scientist Award
- New York State Spinal Cord Injury Research Board
- Boehringer Ingelheim Fonds
- Paralysis Project of America
- National Institute of Mental Health [K99]
During development, axon growth rates are precisely regulated to provide temporal control over pathfinding(1,2). The precise temporal regulation of axonal growth is a key step in the formation of functional synapses and the proper patterning of the nervous system. The rate of axonal elongation is increased by factors such as netrin-1 and nerve growth factor (NGF), which stimulate axon outgrowth using incompletely defined pathways. To clarify the mechanism of netrin-1- and NGF-stimulated axon growth, we explored the role of local protein translation. We found that intra-axonal protein translation is required for stimulated, but not basal, axon outgrowth. To identify the mechanism of translation-dependent outgrowth, we examined the PAR complex, a cytoskeleton regulator(3). We found that the PAR complex, like local translation, is required for stimulated, but not basal, outgrowth. Par3 mRNA is localized to developing axons, and NGF and netrin-1 trigger its local translation. Selective ablation of Par3 mRNA from axons abolishes the outgrowth-promoting effect of NGF. These results identify a new role for local translation and the PAR complex in axonal outgrowth.
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