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Fig. 10. Activation of Smad2 at gastrula stages in the neural plate leads to
defective neural development in Xenopus. (A) Activation of
GR-Smad2 (0.2-0.5 ng) at mid-gastrula stages (stage 11) in the neural tissue
induced neural defects in frog tadpoles. Embryos showed reduced head
structures and malformed or missing eyes. Embryos without DEX treatment
developed normally. (B) Histological analyses indicated that neural
development at both anterior (upper panels) and posterior (lower panels) trunk
levels was defective when Smad2 signaling was activated. The neural tube was
disrupted and ectopic notochord (yellow arrowhead) and mesenchyme (red
arrowhead) were observed in the neural derivatives. (C) In situ
hybridization demonstrated that Sox2 was reduced and split from the midline
and Otx2 was reduced, but the neural crest marker Twist and the muscle marker
MyoD were unaffected. All embryos were viewed from the lateral side with the
anterior to the left, except the second column of Sox2 in panel C, which was
viewed from the dorsal direction.
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