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Fig. 7. Rhombomere 5-specific Wnt8b function is required for the maintenance of
otic fate. (A-D) Assessed by morphology, otic vesicles are reduced
in fgf3 (C) and tcf2 (D) single mutants compared to
wild-type embryos (A), but not as much as in RA-depleted embryos (B).
(E) Loss of both fgf3 and tcf2 together results in
otic vesicles that form only one otolith, as is observed in RA-depleted
embryos (B). (F,G) Expression of dlx3b in the dorsal
half of the otocyst at 22 hpf is lost in embryos depleted of RA signaling.
(H-J) In control embryos at 22 hpf, wnt8b expression can be
detected in the midbrain-hindbrain boundary, in r3 and in r5 (H), whereas
tcf2 mutants (I) and RA-depleted embryos (J) show wnt8b in
the midbrain-hindbrain boundary and in r3, but not in r5. (K-N)
Inactivation of Wnt8b in wild-type embryos by morpholino injection (MO, N)
leads to a reduced ear size (labeled with stm at 22 hpf), similar to
the size observed in fgf3 mutants (M), compared to untreated wild
type (K); however, the size reduction is not as severe as in embryos depleted
of RA signaling (L). Loss of Wnt8b function in fgf3 mutants
(O) produces reduced otic vesicles comparable to RA-depleted embryos
(L). (A-G) Lateral views with anterior to the left and dorsal towards the top.
(H-O) Dorsal views with anterior towards the top. Scale bar: 35 µm for A-E
and H-O; 20 µm for F,G.
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