C Role of the Wnt Pathway in Regulating EpSC Quiescence and Activation

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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