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Fig. 2. Neural induction by inhibitors of Smad1 and Smad2 signaling occurs in the absence of the mesoderm in Xenopus. Double in situ hybridizations showed that neural marker induction in embryos injected with tActRIIB, Smad7 or Ski occurred in the absence of the mesodermal markers Chordin and MyoD. The red speckled staining is from the injected lineage tracer. |
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Fig. 7. Activation of Smad2 signaling converts neural tissue to neural crest and mesodermal tissues in Xenopus. (A) In the absence of DEX, leaky GR-Smad2 activity was sufficient for neural crest induction, but not sufficient for inhibition of neural markers or induction of mesodermal genes. Activation of GR-Smad2 by DEX (2 μM) at mid-gastrula stages led to inhibition of Sox2 and Sox3 and simultaneous induction of the mesodermal markers MyoD and Chordin in the neural plate (seen more clearly in Fig. 7B and Fig. 8). GR-Smad2 RNA (0.1-0.2 ng) was used. The embryos were orientated with the head toward the left and viewed from the dorsal side. (B) Induction of mesodermal markers by activated GR-Smad2 occurred in the neural plate, as shown in transversely bisected (top) or sectioned (bottom) embryos. |
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Fig. 8. The ability to inhibit neural markers by activated Smad2 attenuates during gastrulation. Treatment of Xenopus embryos expressing GR-Smad2 with DEX at different stages during gastrulation showed that activated GR-Smad2 lost its neural inhibitory activity by the end of gastrulation, at which stages it also failed to induce mesoderm in the neural plate. All the embryos were viewed from the dorsal side with the anterior to the left. |