Tissue damage in humans triggers a well-characterized response marked by rapid blood clotting and a recruitment of epidermal cells to the injury. When you remove a scab, you're also removing some of the newly regenerated tissues growing underneath, thereby interfering with the healing process. Many different cell types and proteins have been linked to the repair process, but the complexity of the mammalian wound response has challenged efforts to determine their individual roles.

Michael Galko and Mark Krasnow of Stanford University turned to the quintessential genetics organism, Drosophila melanogaster, to create a novel system for studying wound healing. After stabbing fruitfly larvae with a needle to create a nonfatal puncture wound, the researchers observed the familiar blood clotting and spreading of epidermal cells to promote healing.

Since this epidermal spreading resembles that seen during a well-studied developmental stage of the fruitfly, the authors looked at the roles of specific genes to shed light on the cellular events of healing. Indeed, they found that one particular cell signaling pathway was activated during the peak hours of wound healing. Inhibiting the pathway in fly mutants had dramatic effects on the wound-healing process. The early stages of healing--including plug and scab formation--weren't affected, but epidermal spreading to regenerate the intact epidermis was either blocked or defective. In contrast, larvae with defects in a gene required for the generation of crystal cells--a type of blood cell implicated in processes linked to scab formation--could not properly form scabs. In these scabless wounds, cells at the wound's margin sta
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Contact: Mark Patterson
mpatterson@plos.org
44-122-349-4495
Public Library of Science
20-Jul-2004