The choice between quiescence and activation of EpSCs, whether in the interfollicular epidermis or the hair follicle bulge, involves the Wnt signal transduction pathway ending in Tcf/Lef1, which also operates in the embryonic development of epidermal structures (Gat et al., 1998; Zhu and Watt, 1999; Das Gupta and Fuchs, 1999). The Wnt3 gene is expressed in developing and mature hair follicles and its receptor, Disheveled 2 (Dvl2) is expressed in a subset of cells in the outer root sheath and in precursor cells of the hair shaft (Millar et al., 1999). Overexpression of both Wnt3 and Dvl2 give a short-hair and cyclical balding phenotype in mice resulting from structural defects and an abnormal profile of protein expression in the hair shaft. In quiescent telogen hair follicles, Lef-1 represses the activity of EpSCs, because active GSK-3P prevents P-catenin from dissociating from the APC protein, which degrades P-catenin. At anagen, Wnt proteins activate EpSCs by inhibiting the enzyme GSK-3P through Dvl2, allowing
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