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Fgf Signaling Induces Posterior Neuroectoderm Independently of Bmp Signaling Inhibition

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Rentzsch,  Fabian
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Bakkers,  Jeroen
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Kramer,  Carina
Spemann Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191086

Hammerschmidt,  Matthias
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Rentzsch, F., Bakkers, J., Kramer, C., & Hammerschmidt, M. (2004). Fgf Signaling Induces Posterior Neuroectoderm Independently of Bmp Signaling Inhibition. Developmental Dynamics, 231, 750-757.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9493-A
Abstract
Whereas according to the neural default model, neural specification is induced by extracellular inhibitors of bone morphogenetic proteins (Bmps), the role of fibroblast growth factors (Fgfs) during neural induction is heavily debated. Here, we show that, in zebrafish embryos, Bmps and Fgfs play differential roles during the induction and patterning of the anterior vs. the posterior neuroectoderm. Induction of anterior neuroectoderm, giving rise to fore- and midbrain, is accomplished by Bmp inhibition, with Fgfs playing a moderate posteriorizing/patterning role, possibly by blocking Bmp signaling at the level of Smad proteins. In contrast, in the posterior-most neuroectoderm, which is located in marginal regions of the early gastrula embryo to give rise to spinal cord and hindbrain, Fgfs play a neural-inducing rather than a neural-patterning role. This Fgf-dependent posterior neural induction takes place during late blastula and early gastrula stages, after mesoderm has been induced and cannot be blocked by Bmps or the Bmp target gene and downstream effector ΔNp63α, indicating that here, Fgfs act independently of Bmp signaling inhibition.