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
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • Phenotype
  • Animals
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Oligonucleotides, Antisense/genetics
  • Oligonucleotides, Antisense/metabolism
  • Neurons/cytology
  • Neurons/physiology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Cell Proliferation
  • Embryo, Nonmammalian/anatomy & histology
  • Embryo, Nonmammalian/physiology
  • Embryonic Structures/anatomy & histology
  • Embryonic Structures/physiology*
  • Gene Expression Regulation, Developmental
  • Neural Crest/cytology
  • Neural Crest/embryology*
  • In Situ Hybridization
  • Cell Survival
(all 25)
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
Figure Gallery (8 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b380
    Deficiency
    x8
      Deficiency
      1 - 2 of 2
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      msx1aMO1-msx1aMRPHLNO
      msx1bMO4-msx1bMRPHLNO
      msx3MO1-msx3MRPHLNO
      1 - 3 of 3
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      Fish
      Antibodies
      No data available
      Orthology
      No data available
      Engineered Foreign Genes
      No data available
      Mapping
      Entity Type Entity Symbol Location
      Featurex8Chr: 1 Details
      GENElef1Chr: 1 Details
      GENEmsx1bChr: 1 Details
      1 - 3 of 3
      Show