Many of the defects in the skin of these mice did not seem to be merely a consequence of defective intercellular adhesion. To demonstrate this, the researchers looked at skin in a mouse in which the molecule with the same ascribed function in the desmosome cell junction was missing. Though both animals showed severe defects in adhesion, the skin in the desmosome knockout did not show the changes in cell cycle control. Exactly how this happens is still not clear, but their studies indicate that the signaling pathway of a cell that responds to growth factors intersects the pathway that regulates intercellular junction formation. At the crossroads of this junction appears to be alpha-catenin.
Skin cells respond to changes in their immediate environment.
During this process, the cells must keep the number of intercellular contacts to a minimum so that they are free to move in to the wound site. Elaine Fuchs, Ph.D., is Amgen Professor of Molecular Genetics and Cell Biology and a Howard Hughes Investigator at the University of Chicago. Additional authors of the paper include Valera Vasioukhin, Ph.D., Christoph Bauer, Ph.D., Linda Degenstein, and Bart Wise, Ph.D., of the University of Chicago. This work was supported by grants from the National Institutes of Health and from the National Cancer Institute. All rights reserved.