Jamming the epidermal growth factor (EGF) receptor allows severed neurons to regenerate.1 "It's a surprising finding," says Martin Schwab of the University of Zurich, as activation of the EGF receptor is normally associated with proliferation and growth of cells.
Previous research that sought to explain why mammalian axons fail to regenerate in the wounded brain or spinal cord found several inhibitory cues that prevent healing. The culprits include proteins associated with myelin and proteoglycans released by the glial scar that forms after neural injury. In a search for a signal that might override this chemical blockade, a group led by Zhigang He of Children's Hospital in Boston cultured neurons on a myelin substrate.
They screened approximately 400 candidate compounds, looking for those that could promote growth in this hostile environment. When exposed to a subset of the molecules that shared the ability to shut down the EGF receptor, neurons sprouted extensions called neurites, the first step to extending axons. In this case, "activation of the receptor is involved in blocking things, not in stimulating growth," says coauthor Marc Tessier-Lavigne, senior vice president for research at Genentech in South San Francisco. "It's an unexpected role for the EGF receptor."