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Fig. S4. FoxD3 rescue of axis formation in embryos injected with VP16-FoxD3 or FoxD3MO. The inhibition of axis formation by VP16-FoxD3 and FoxD3MO is predicted to result from a specific block of endogenous FoxD3 function. To determine the specificity of FoxD3 inhibition, FoxD3 was co-injected with VP16-FoxD3 or FoxD3MO in an attempt to rescue axis formation. At the four-cell stage, both dorsal blastomeres were injected with VP16-FoxD3 or FoxD3MO alone, or in combination with FoxD3 RNA, and axis formation was assessed at the tadpole stage. Whereas the majority of VP16-FoxD3-injected embryos had severe axial defects, only a minority displayed defects with FoxD3 co-injection (C,D). Similarly, the axial defects caused by FoxD3MO were rescued by FoxD3 RNA lacking the antisense target sequence (FoxD3-utr), but not by FoxD3 RNA containing the target sequence (FoxD3+utr) (E,F,H). As controls, injection of both dorsal blastomeres with FoxD3 RNA alone (B) or mismatch MO (G) did not perturb axis formation, by comparison with control (A). See Table 1 for quantification.

Image published in: Steiner AB et al. (2006)

Copyright © 2006. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.

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