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Fig. 2. Hh-independent target gene expression in igu embryos. (A-D) In
control wild-type embryos treated with 5% DMSO, expression patterns of
ptc1 at 14 hpf (A), myod at 14 hpf (B), en1 at
30hpf (C), ptc1 at 30 hpf (D) and nk2.2 at 30 hpf (E) are
all normal. (F-J) Wild-type embryos treated with cyclopamine. Expression of
ptc1 at 14 hpf (F), adaxial myod at 14 hpf (G), en1
at 30hpf (H), ptc1 at 30 hpf (I) and nk2.2 (J) at 30 hpf, is
efficiently suppressed. Note that a low level of ptc1 expression in
the neural tube in I appears to be independent of Smo-mediated Hh signaling,
since similar ptc1 activation is seen in smu/smo mutants at
30 hpf (data not shown). (K-O) igu embryos treated with cyclopamine.
A broad activation of ptc1 expression in igu mutants at 14
hpf (K) is not affected by cyclopamine. Arrows indicate the adaxial cells.
Expression of myod in adaxial cells is indistinguishable from normal
wild-type embryos, and is not affected by cyclopamine (L). Likewise,
en1 (M) and ptc1 (N) expression in 30 hpf embryos is not
affected by cyclopamine. Despite the defect of nk2.2 expression in
igu mutants, the residual expression of nk2.2 in the neural
tube is not eliminated by cyclopamine (O). The genotypes of these embryos were
confirmed using tightly linked PCR-based genetic markers after in situ
staining.
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