Figure 2.

Effect of physiological and non-physiological ROS on axonal growth cone organization. Oxidative stress (due to mitochondrial dysfunction, Sema3A/Plexin signaling and MICAL1 activation, neurodegenerative disorders, among others) induces the collapse of the axonal growth cones of neurons. In contrast, down-regulation of ROS synthesis, particularly due to NOX inhibition as well as Chronic Granulomatous Disease (CGD), decreases the F-actin content at the growth cone and affect filopodial dynamics by decreasing the number and length of filopodia at the axonal growth cone. Physiological concentrations of ROS, principally maintained by NOX enzymes and basal mitochondrial activity, are needed for a proper organization of the growth cones. In this context, the implicances for vesicular trafficking due to altered cytoskeleton dynamics has not been explored.