PUBLICATION

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

Authors
Phillips, B.T., Kwon, H.J., Melton, C., Houghtaling, P., Fritz, A., and Riley, B.B.
ID
ZDB-PUB-060501-3
Date
2006
Source
Developmental Biology   294(2): 376-390 (Journal)
Registered Authors
Kwon, Hye-Joo, Riley, Bruce
Keywords
msx, dlx, eya, six, foxd3, snail2, sox10, Placode, Neural crest
MeSH Terms
  • Animals
  • Cell Proliferation
  • Cell Survival
  • Embryo, Nonmammalian/anatomy & histology
  • Embryo, Nonmammalian/physiology
  • Embryonic Structures/anatomy & histology
  • Embryonic Structures/physiology*
  • Gene Expression Regulation, Developmental
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • In Situ Hybridization
  • Neural Crest/cytology
  • Neural Crest/embryology*
  • Neurons/cytology
  • Neurons/physiology*
  • Oligonucleotides, Antisense/genetics
  • Oligonucleotides, Antisense/metabolism
  • Phenotype
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
16631154 Full text @ Dev. Biol.
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.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes