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Vol. 15, No. 13, pp. 1688-1705, July 1, 2001
Howard Hughes Medical Institute, Department of Molecular Genetics
and Cell Biology, The University of Chicago,
Chicago, Illinois 60637, USA
In skin, multipotent stem cells generate the keratinocytes of the
epidermis, sebaceous gland, and hair follicles. In this paper, we show
that Tcf3 and Lef1 control these differentiation lineages. In contrast
to Lef1, which requires Wnt signaling and stabilized 
-catenin to
express the hair-specific keratin genes and control hair
differentiation, Tcf3 can act independently of its -catenin
interacting domain to suppress features of epidermal terminal
differentiation, in which Tcf3 is normally shut off, and promote
features of the follicle outer root sheath (ORS) and multipotent stem
cells (bulge), the compartments which naturally express Tcf3. These
aspects of Tcf3's action are dependent on its DNA binding and Groucho
repressor-binding domains. In the absence of its -catenin
interacting domain, Lef1's behavior (
NLef1) seems to be markedly
distinct from that of NTcf3. NLef1 does not suppress epidermal
differentiation and promote ORS/bulge differentiation, but rather
suppresses hair differentiation and gives rise to sebocyte differentiation. Taken together, these findings provide powerful evidence that the status of Tcf3/Lef complexes has a key role in
controlling cell fate lineages in multipotent skin stem cells.
[Key Words:
-Catenin; groucho; CtBP; Wnt/wingless; hair follicle]
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