Fig. 9. DV patterning of the early zebrafish embryo. (A) Two levels of regulation of the morphogenetic Bmp activity gradient. First, the action of Bmp proteins (dark blue squares) is inhibited by chordin and noggin (red), which bind Bmps and prevent them from interacting with their receptors. Second, Fgfs affect the DV patterning by restricting the domain of Bmp gene expression (light blue). Fgf signals are modulated by feedback-inhibitors such as Spry2. The combined regulation of Bmp gene expression and Bmp protein activity results in the generation of a Bmp activity gradient (dark blue) that determines the identity of cells along the DV axis. Cells that experience high levels of Bmp activity will adopt a ventral (e.g. epidermal, green; ventral, V) fate, cells that experience a low Bmp activity a more dorsal (e.g. anterior neurectodermal, yellow; dorsal, D) fate. (B) Noggin overexpression does not affect early Bmp gene expression but abolishes Bmp activity by complexing all available Bmp molecules. As a result, the ventral epidermis is lost, to the benefit of the dorsal neurectoderm. (C) Fgf overexpression abolishes Bmp gene expression and therefore also Bmp activity. As for Noggin-injected embryos, the ventral epidermis is lost at the expense of the dorsal neurectoderm. (D) Loss of function of the Fgf-signalling antagonist spry2 causes an upregulation of endogenous Fgf signalling and a decrease of the Bmp transcription domain. The dorsal neurectoderm is expanded at the expense of the epidermis. (E) Following inhibition of Fgf signalling, Bmp gene transcripts are expressed throughout the embryo with the exception of the dorsalmost marginal blastomeres. As a consequence, the ventral epidermis expands while the dorsal neurectoderm is severely reduced in size. (F) Overexpression of Noggin in Fgf-depleted embryos inactivates Bmp proteins. Consequently, all cells adopt a dorsal neurectodermal fate.