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Fig. 3. Decreased Gli activator function and/or increased Gli repressor function
represses ectopic Hh target gene expression in igu embryos. (A-I)
Introduction of dtr/gli1 mutant alleles into the igu genetic
background suppressed ectopic Hh target gene expressions in somites. In
dtr/gli1–/– embryos (A-C), the expression of
nk2.2 and ptc1 is reduced, but en1 expression is
normal. In dtr/gli1–/+;igu–/–
embryos (D-F), nk2.2 expression is similar to
dtr/gli1–/– embryos (D), with no
nk2.2 expression in the posterior neural tube. By contrast, the
expression of en1 (E) and ptc1 (F) are similar to that seen
in igu–/– mutants; however, en1
expression is reduced in anterior somites. In
dtr/gli1–/–;igu–/–
embryos (G-I), the decrease of en1 and ptc1 is more evident
(H,I), and the overall phenotype including nk2.2 (G) is stronger than
in dtr/gli1–/– embryos. Insets show higher
magnification views of ptc1 expression in the trunk region. (J-O) A
drastic reduction of Hh target gene expression is caused by the introduction
of a yot/gli2 mutant allele into the igu genetic background.
One copy of yot/gli2 completely suppressed ectopic target gene
expression (M-O), and the resulting phenotype is similar to or even stronger
than that seen in yot/gli2–/– embryos (J-L).
An arrowhead marks a spot of nk2.2 expression, which is consistently
seen only in yot/gli2–/– embryos (J) but not
in yot/gli2–/+;igu–/– embryos
(M). The genotypes of these embryos were confirmed by PCR after in situ
staining.
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