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Fig. 8. Gli1 expression and activity are not under the control of Hh signaling
during IZ formation. (A-F) Expression of gli1 is
unaffected upon cyclopamine (A,C,E) or mock treatment (B,D,F) applied between
the dome stage and the stage of analysis [70% epiboly (A,B), tailbud (C,D) and
3 somites (E,F)]. (G,H) Expression of myoD (blue) and
pax2.1 (red) on 6-somite zebrafish embryos (dorsal views, anterior
left) upon cyclopamine treatment (H) as compared with mock treatment (G). The
same cyclopamine concentration was used as in A,C,E; treatment between 50%
epiboly and 6 somites. myoD is strongly decreased in adaxial cells
(H, white arrowhead; compare with G, blue arrow). (I-N) Expression of
neurog1 (blue) and pax2.1 (red) at the 3- to 5-somite stage
(anterior up) is unaffected upon cyclopamine treatment applied at any stage
between dome and 3-5 somites (J-L, compare with N). Cyclopmaine also does not
rescue the effects of her5GripNA injections (M, compare with I), in
contrast to the effect of blocking Gli1 activity (see
Fig. 7F). (O,P)
Expression of neurog1 (blue) and pax2.1 (red) at 3-5 somites
is unaffected by blockade of Hh signaling via overexpression of
Patched
loop (O, compare with control P).
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