Cellular, Molecular and Epigenetic control of axon regeneration
Permanent disabilities following central nervous system (CNS) injuries result from the failure of injured axons to regenerate and re-build functional connections. The poor intrinsic regenerative capacity of mature CNS neurons is a major contributor to the regeneration failure and remains a major problem in neurobiology. In contrast to CNS neurons, peripheral sensory neurons successfully regenerate injured axons. However, functional recovery in the peripheral nervous system (PNS) is often incomplete, especially after complete nerve transection or when axons need to re-grow long distances to reach their targets. Peripheral nerve injury can also result in chronic pain. The primary goal in the Cavalli lab is to reveal the principles and mechanisms by which injured sensory neurons re-activate a pro-regenerative program following axon injury and identify potential targets for future treatment of CNS injuries and severe PNS injuries. We use biochemical, molecular, cell biological, imaging, behavioral, genetic and epigenetic approaches in the mouse model system to elucidate the mechanisms controlling axon regeneration.