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Fig. 7. Proposed model for the role of Wnt signaling in mediating the otic
placode-epidermis fate decision and dorsal otocyst cell fates. (A)
Summary of the ß-catenin loss-of-function (CKO) and gain-of-function
(cAct) phenotypes. Control: Wnt-TCF/Lef is activated (magenta) in
Pax2+ surface ectoderm by Wnt (blue) from hindbrain (HB) to
delineate the size of the otic placode (dark blue). Pax2+
cells that do not receive Wnt signals differentiate as epidermis (gray). In
CKO, in the absence of Wnt signaling, epidermis (gray) is expanded at the
expense of the otic placode. In cAct, stabilized ß-catenin activates
Wnt-responsive genes in a wide region of the surface ectoderm, thus expanding
the otic placode at the expense of epidermis. Ovals in the top panels
represent the otic placode. A, anterior; P, posterior. Lower panels represent
a transverse section at the level shown in the top panels as a broken line.
The strength of the Wnt-mediated response is shown as graph. (B) A
model of the induction and polarization of the otic placode. E8.0:
Pax2 in the surface ectoderm (SE) is induced by Fgf signaling from
underlying tissues and/or the hindbrain. E8.5: Wnt signaling from rhombomere
(r) 4 directs the medial-most region of the Pax2+ ectoderm
to an otic placode fate and activates expression of dorsal otic markers such
as Dlx5. Cells that do not receive Wnt signaling in the
Pax2+ ectoderm are directed to an epidermal fate and
express epidermal-specific genes such as Foxi2. E8.75+: As
the otic placode invaginates, signals from the ventral midline (orange) such
as Shh activate expression of ventral otocyst genes and repress dorsal cell
fates (Riccomagno et al.,
2002; Riccomagno et al.,
2005).
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