These experiments show that the phenotype of the FCN morphant is specific to a loss of BMP antagonism. Instead, in a second rescue experiment, we subsequently injected additional MOs that are targeted against BMP4 and BMP7 (to attenuate BMP signaling) into half of the FCN morphant embryo and this results in a partial rescue of the neural plate ( Figures 4K–4M). Also, if the phenotype of the triple morphant is due to MO toxicity, then additional MOs should exacerbate the effect. Triple morphants injected with noggin mRNA develop rescued neural plates and dorsal mesoderm ( Figures 4A–4J ). First the FCN morphants were secondarily injected with pufferfish noggin mRNA, whose sequence is different from Xenopus. In order to show that these results are specific to a reduction in BMP antagonism, we performed two rescue experiments. In addition, our results show that neural specification requires the continuous activity of BMP antagonists from blastula through gastrula stages. We conclude that BMP antagonists are required for formation of the neural plate and dorsal mesoderm. We demonstrate that this results in catastrophic failure of dorsal development and expansion of ventral and posterior fates. Here, we deplete the function of three BMP antagonists, chordin, noggin, and follistatin, in Xenopus tropicalis. However, at least five BMP antagonists are specifically expressed in the organizer, and all can mimic aspects of organizer function, suggesting overlapping functions. Thus, the role of BMP antagonists may be limited to fine tuning the size of the dorsal domain. Transplanted Spemann’s organizer induces dorsal embryonic cell fates such as the nervous system and somites, but in normal development, elimination of individual organizer signals (such as the bone morphogenetic protein antagonists) has surprisingly modest effects on these tissues.
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