期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 290, 期 23, 页码 14765-14775出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.622753
关键词
-
资金
- NINDS/National Institutes of Health [R01 NS082446]
- National Research Foundation of Korea [NRF-2012R1A6A3A03039290]
Injured peripheral neurons successfully activate a pro-regenerative program to enable axon regeneration and functional recovery. The microtubule-dependent retrograde transport of injury signals from the lesion site in the axon back to the cell soma stimulates the increased growth capacity of injured neurons. However, the mechanisms initiating this retrograde transport remain poorly understood. Here we show that tubulin-tyrosine ligase (TTL) is required to increase the levels of tyrosinated alpha-tubulin at the axon injury site and plays an important role in injury signaling. Preventing the injury-induced increase in tyrosinated alpha-tubulin by knocking down TTL impairs retrograde organelle transport and delays activation of the pro-regenerative transcription factor c-Jun. In the absence of TTL, axon regeneration is reduced severely. We propose a model in which TTL increases the levels of tyrosinated alpha-tubulin locally at the injury site to facilitate the retrograde transport of injury signals that are required to activate a pro-regenerative program.
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