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Fig. 6. Components of the Notch pathway participate in a Wnt3a-dependent pathway
that controls laterality and somitogenesis. (A-D) Whole-mount in situ
hybridization analysis of Dll1 expression in E8 wild-type (A,C) and
Wnt3a-/- (B,D) embryos. Dll1 expression in the
psm surrounds the wild-type node (C), but only abuts the posteriormost node in
a Wnt3a-/- embryo (D). The lines in A and B, and ovals in
C and D, indicate the location of the node. (E-H) Histological sections of
wild-type neonatal heart (E), and three examples of cardiac laterality defects
in compound Wnt3avt; Dll1 mutants, including PTA (arrow,
F), TGA (G) and VSD (arrow, H). (I,J) Axin2 expression in the streak,
psm and in an anterior stripe (presomite 0) in wild-type one-somite embryos
(I), was downregulated in Wnt3a-/- mutants and no psm
stripes were observed (J). (K,L) Two color whole-mount in situ hybridization
on four-somite stage embryos, illustrating (K) cycling Lfng (purple)
and Nodal expression (orange) in the wild-type left LPM. Dynamic
Lfng expression was not observed in the absence of Wnt3a, as
only a single psm stripe was observed in the Wnt3a mutants (L). Nodal
was not expressed in the mutant LPM at these stages.
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