| First Author | Cho Y | Year | 2013 |
| Journal | Cell | Volume | 155 |
| Issue | 4 | Pages | 894-908 |
| PubMed ID | 24209626 | Mgi Jnum | J:205287 |
| Mgi Id | MGI:5544524 | Doi | 10.1016/j.cell.2013.10.004 |
| Citation | Cho Y, et al. (2013) Injury-induced HDAC5 nuclear export is essential for axon regeneration. Cell 155(4):894-908 |
| abstractText | Reactivation of a silent transcriptional program is a critical step in successful axon regeneration following injury. Yet how such a program is unlocked after injury remains largely unexplored. We found that axon injury in peripheral sensory neurons elicits a back-propagating calcium wave that invades the soma and causes nuclear export of HDAC5 in a PKCmu-dependent manner. Injury-induced HDAC5 nuclear export enhances histone acetylation to activate a proregenerative gene-expression program. HDAC5 nuclear export is required for axon regeneration, as expression of a nuclear-trapped HDAC5 mutant prevents axon regeneration, whereas enhancing HDAC5 nuclear export promotes axon regeneration in vitro and in vivo. Components of this HDAC5 pathway failed to be activated in a model of central nervous system injury. These studies reveal a signaling mechanism from the axon injury site to the soma that controls neuronal growth competence and suggest a role for HDAC5 as a transcriptional switch controlling axon regeneration. |
