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Fig. 3. The MDT is reduced in embryos deficient for Hh signalling.
(A) Inhibition of Hh signalling by cyclopamine treatment (70 µm)
from 10-somites to 30 hours leads to a strong reduction of dlx2a
expression anterior to the ZLI and dbx1a posterior to the ZLI
(B). ptc1 expression is not detectable in these embryos
(B'). Weaker phenotype observed with treatment between 20 somites and 30
hours (C; dlx2a-positive prethalamus is marked by blue bracket
and dbx1a by yellow bracket), although ptc1 expression is
still undetectable (C'). After 24 hpf, inhibition of Hh signalling has
no detected effect (D) compared with wild-type siblings (A). Asterisks
indicate the ZLI (A-D). Analysis of the smu phenotype reveals Hh
dependency for gene expression in the MDT (E-H').
dlx2a is not detectable in the prethalamus (E,E', blue arrow),
lhx5 expression is downregulated (F,F', blue arrow),
dbx1a is absent form the thalamus (G,G'; yellow arrow), in
contrast to the ZLI (asterisk). Similarly, emx2 is downregulated
(H,H'; yellow arrow). Tec, tectum; Teg, tegmentum; Tel,
telencephalon.
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