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Zebrafish msxB, msxC and msxE function together to refine the neural–nonneural border and regulate cranial placodes and neural crest development
Journal article   Open access   Peer reviewed

Zebrafish msxB, msxC and msxE function together to refine the neural–nonneural border and regulate cranial placodes and neural crest development

Bryan T Phillips, Hye-Joo Kwon, Colt Melton, Paul Houghtaling, Andreas Fritz and Bruce B Riley
Developmental biology, Vol.294(2), pp.376-390
2006
DOI: 10.1016/j.ydbio.2006.03.001
PMID: 16631154
url
https://doi.org/10.1016/j.ydbio.2006.03.001View
Published (Version of record) Open Access

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.
dlx eya foxd3 msx Neural crest Placode six snail2 sox10

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