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Fig. 8. Estrogen signaling is intact in Wnt5a mutant grafts. In situ
hybridization for Esr1 (A-F), Wnt5a (G-J), Pgr
(K-P) and Msx1 (Q-T) from host uteri and grafts grown in saline or
DES conditions, as indicated at the bottom. Genotypes are indicated on the
left. Esr1 expression increases to very high levels in adult mice
after ovariectomy (A) but is repressed after prolonged exposure to DES, except
in the epithelium and the smooth muscle layer (B). Although lower in
3-week-old grafts, Esr1 expression is similarly regulated in both
control Wnt5a+/– (C,D) and
Wnt5a-/- grafts (E,F). Wnt5a is downregulated in
the stroma and activated in the epithelium and smooth muscle, and
Wnt5a mutant transcript is correctly regulated even in absence of
Wnt5a product (H,J). Pgr gene regulation is also identical
in control and mutant grafts although Pgr is not downregulated in the
epithelium from grafts (N,P) as in the host (L), probably because of stage
difference between immature 3-week-old grafts and sexually mature host uterus.
Msx1 is repressed by DES in both control (R) and Wnt5a
mutant grafts (T).
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