|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
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.
|
