ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS.
Neuron
; 103(6): 1073-1085.e6, 2019 09 25.
Article
de En
| MEDLINE
| ID: mdl-31400829
ABSTRACT
Injured axons fail to regenerate in the adult CNS, which contrasts with their vigorous growth during embryonic development. We explored the potential of re-initiating axon extension after injury by reactivating the molecular mechanisms that drive morphogenetic transformation of neurons during development. Genetic loss- and gain-of-function experiments followed by time-lapse microscopy, in vivo imaging, and whole-mount analysis show that axon regeneration is fueled by elevated actin turnover. Actin depolymerizing factor (ADF)/cofilin controls actin turnover to sustain axon regeneration after spinal cord injury through its actin-severing activity. This pinpoints ADF/cofilin as a key regulator of axon growth competence, irrespective of developmental stage. These findings reveal the central role of actin dynamics regulation in this process and elucidate a core mechanism underlying axon growth after CNS trauma. Thereby, neurons maintain the capacity to stimulate developmental programs during adult life, expanding their potential for plasticity. Thus, actin turnover is a key process for future regenerative interventions.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Traumatismes de la moelle épinière
/
Axones
/
Actines
/
Cônes de croissance
/
Cofiline-1
/
Cofiline-2
/
Destrine
/
Régénération nerveuse
Limites:
Animals
Langue:
En
Journal:
Neuron
Sujet du journal:
NEUROLOGIA
Année:
2019
Type de document:
Article
Pays d'affiliation:
Allemagne