ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS

2019-09-17

Recently scientists from German Center for Neurodegenerative Diseases (DZNE) published their big discovery on Neuron.
Heres the point of their discovery: 
.Elevated actin turnover is essential for regenerative growth.
.ADF/cofilin activity increases during conditioning-mediated regeneration.
.ADF/cofilin is necessary and sufficient for axon regeneration.
The severing activity of ADF/cofilin is critical for axon regeneration. Injured axons fail to regenerate in the adult CNS, which contrasts with their vigorous growth during embryonic development. 
Scientists 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 vivoimaging, 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.
 
Sherry