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Fig. 1. vhnf1 acts downstream of RA to activate val. (A,B)
vhnf1 (blue) is expressed posterior to the r4/5 boundary at about
10.7 hpf in control EtOH-treated embryos (A, krox20 expression in r3
and r5 is in red), and is expanded in its AP extent in the hindbrain of
embryos treated with 10–7 M all-trans RA (B). (C,D) Treating
embryos with 10–5 M AGN193109, a pan-RAR antagonist, from
4.5-11 hpf blocks vhnf1 expression and r5 specification (D) compared
with DMSO-treated controls (C). (E,F) Wild-type embryos (E) exhibit robust
vhnf1 expression by 9.5-10 hpf compared with their
nls– siblings (F). (G-J) Embryos were treated with
2% DMSO or 10–5 M AGN193109, either alone or in combination
with overexpression of vhnf1 (35 pg mRNA) as shown. (G) DMSO-treated
controls show normal val expression (blue) in r5 and r6 at
approximately 11.7 hpf and this expression is inhibited by treatment with AGN
193109 (H). Overexpression of vhnf1 causes a slight expansion of
val expression in untreated embryos (I) and rescues val
expression in AGN193109-treated embryos (J). A-F are shown as dorsal views
with anterior to the left (A-D) or to the top (E,F).
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