Abstract
The zebrafish
muscle segment homeobox genes
msxB,
msxC and
msxE are expressed in partially overlapping domains in the neural crest and preplacodal ectoderm. We examined the roles of these
msx genes in early development. Disrupting individual
msx genes causes modest variable defects, whereas disrupting all three produces a reproducible severe phenotype, suggesting functional redundancy. Neural crest differentiation is blocked at an early stage. Preplacodal development begins normally, but placodes arising from the
msx expression domain later show elevated apoptosis and are reduced in size. Cell proliferation is normal in these tissues. Unexpectedly, Msx-deficient embryos become ventralized by late gastrulation whereas misexpression of
msxB dorsalizes the embryo. These effects appear to involve Distal-less (Dlx) protein activity, as loss of
dlx3b and
dlx4b suppresses ventralization in Msx-depleted embryos. At the same time, Msx-depletion restores normal preplacodal gene expression to
dlx3b-dlx4b mutants. These data suggest that mutual antagonism between Msx and Dlx proteins achieves a balance of function required for normal preplacodal differentiation and placement of the neural–nonneural border.