| First Author | Tedeschi A | Year | 2019 |
| Journal | Neuron | Volume | 103 |
| Issue | 6 | Pages | 1073-1085.e6 |
| PubMed ID | 31400829 | Mgi Jnum | J:284543 |
| Mgi Id | MGI:6381951 | Doi | 10.1016/j.neuron.2019.07.007 |
| Citation | Tedeschi A, et al. (2019) ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS. Neuron 103(6):1073-1085.e6 |
| abstractText | 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. |
