Schwann cells play a major supporting role in peripheral nerve regeneration following injury. They migrate towards the site of injury, where they provide a guide for regenerating axons. However, the molecular events that control their migration are largely unknown. On , Namgung and colleagues demonstrate that the cyclin-dependent kinase Cdc2, better known for its role controlling cell cycle progression, is necessary for this process. They find that following injury to the sciatic nerve, isolated Schwann cells show elevated Cdc2 expression and enhanced migration. Inhibition of Cdc2 can block this effect, whereas increased Cdc2 expression enhances cell migration. The authors identify caldesmon, an actin-binding protein, as a key Cdc2 kinase substrate. Phosphorylation of caldesmon by Cdc2 alters its subcellular localisation away from the peripheral cytoskeleton to the centre of the cell. They go on to show that inhibition of the Cdc2-caldesmon pathway, using a dominant-negative form of caldesmon, suppresses Schwann cell migration. Their data support an emerging new function of Cdc2 and other Cdk family members in the nervous system and provide insight into the mechanisms of nerve regeneration.
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