TY - JOUR PY - 2012// TI - HDAC5 is a novel injury-regulated tubulin deacetylase controlling axon regeneration JO - EMBO journal A1 - Cho, Yongcheol A1 - Cavalli, Valeria SP - 3063 EP - 3078 VL - 31 IS - 14 N2 - Axon regeneration is an essential process to rebuild functional connections between injured neurons and their targets. Regenerative axonal growth requires alterations in axonal microtubule dynamics, but the signalling mechanisms involved remain incompletely understood. Our results reveal that axon injury induces a gradient of tubulin deacetylation, which is required for axon regeneration both in vitro and in vivo. This injury-induced tubulin deacetylation is specific to peripheral neurons and fails to occur in central neurons. We found that tubulin deacetylation is initiated by calcium influx at the site of injury, and requires protein kinase C-mediated activation of the histone deacetylase 5 (HDAC5). Our findings identify HDAC5 as a novel injury-regulated tubulin deacetylase that plays an essential role in growth cone dynamics and axon regeneration. In addition, our results suggest a mechanism for the spatial control of tubulin modifications that is required for axon regeneration.
Language: en
LA - en SN - 0261-4189 UR - http://dx.doi.org/10.1038/emboj.2012.160 ID - ref1 ER -