Scientists have known for more than 150 years that wounds generate faint electric fields. Most researchers recognize that these fields play some role in wound healing, but just exactly how this worked or which genes were involved in this electric response–called electrotaxis–remained unclear.
Biomedical scientist Min Zhao of the University of Aberdeen in the United Kingdom and colleagues charged at the problem by creating a set of fluorescent markers that lit up when electrical signals set off a biochemical cascade inside the cell. “We saw that the same cascades that control chemotaxis [the response to chemical signals] were also involved in electrotaxis,” says team member Josef Penninger of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences. Chemotaxis is also important in wound healing. The next step was figuring out which genes are involved in a cell’s electrical response. Applying electric fields to artificial wounds in cell culture dishes and real wounds in rodent corneas, the team detected epithelial cells rushing towards the wound center; reversing the field caused the cells to change direction. Then, the team disrupted a gene called p110 gamma in cultured cells. The gene codes for a chemical, called PI(3)K gamma, which is also a key player in chemotaxis. In mutants without p110 gamma, cells did not move to the wound in response to electric signals.
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