"The genes involved in cuticle repair are activated very quickly, within 30 minutes after injury," said Joseph Pearson, a graduate student working under McGinnis and a coauthor of the paper. "They are activated over many cell diameters, most strongly at the boundaries of the wound, suggesting that the grainyhead gene initiates the cuticle repair response after it receives an as-of-yet unidentified signal produced in cells adjacent to the injury."
In its study, Jane's team found that, like their fruit fly counterparts, mice lacking grainyhead have a much more permeable skin than normal mice and have deficient wound repair. Both groups point out in their papers that it is interesting that the regulatory mechanisms for development and repair of the surface barrier in insects and mammals have been conserved, given the differences in the molecular composition of insect cuticle and mammal skin.
"The proteins that link together to form the insect cuticle and stratum corneum--the outer layer of mammal skin--are completely different," says McGinnis. "So it is remarkable that flies and mammals share an ancient conserved pathway to construct and repair the body envelope that protects them from sharp edges and microbes, even though that body envelope is constructed of mostly different molecules."
In their paper, the UCSD researchers state that studying the wound response pathway in fruit flies, which are easy to manipulate genetically, may provide new insight into wound healing in mammals. For example, Mace points out that very little is known how wound tissue stops its growth behavior when the wound is healed. In a
Source:University of California - San Diego