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Fig. 5. (A-D) Tbx2b is regulated by Fz7. (A) TOP-flash assay shows a reduction of
ß-catenin-dependent Tcf activity in fz7 morphants. (B)
Expression of fz7 at 5.3 hpf (cross-section). (C) Expression of a
dn-fz7-EGFP/BAC (red, see Materials and methods) caused the loss of
tbx2b expression (blue) in the eye (arrow). (D) The absence of
fz7 MO/fluorescein-injected cells in the eyes and CNS at 24 hpf is
rescued by co-injection of tbx2b mRNA. (E) Real-time PCR analysis of
Tbx2b and Fz7 morphants showed a decrease in tbx2b and fz7
transcripts in the presence of fz7 MO, but no effect from
tbx2b MO at 5 hpf. n=15 for control, n=7 for
tbx2b MO and n=4 for fz7 MO. (F-I) Rescue of cell
movement defect by transplantation into wild-type host at shield stage.
Wild-type donor cells differentiated into morphologically distinct cells in
the eye (F) and hindbrain (G) by 24 hpf. By contrast, only a few
Tbx2b-deficient cells differentiated into distinct eye (H) and hindbrain (I)
cells (arrowheads).
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