PUBLICATION

Control of muscle cell-type specification in the zebrafish embryo by hedgehog signalling

Authors
Lewis, K.E., Currie, P.D., Roy, S., Schauerte, H., Haffter, P., and Ingham, P.W.
ID
ZDB-PUB-991216-1
Date
1999
Source
Developmental Biology   216(2): 469-480 (Journal)
Registered Authors
Currie, Peter D., Haffter, Pascal, Ingham, Philip, Lewis, Katharine E., Roy, Sudipto, Schauerte, Heike
Keywords
Zebrafish; Patched1; Sonic hedgehog; Gli2; U-type mutants; Muscle fibre type; MyoD; Myosin heavy chain; You; You-too; Sonic you; Chameleon; U-boot; gene control; muscle cell; cell type; cell specificity; signal transduction; sonic hedgehog protein
MeSH Terms
  • Animals
  • Cell Differentiation
  • Fluorescent Antibody Technique
  • Gene Expression Regulation, Developmental
  • Hedgehog Proteins
  • In Situ Hybridization
  • Kruppel-Like Transcription Factors
  • Membrane Proteins/genetics
  • Muscles/embryology*
  • Muscles/metabolism
  • Mutation
  • MyoD Protein/genetics
  • Myosins/metabolism
  • Proteins/metabolism*
  • RNA, Messenger/metabolism
  • Receptors, Cell Surface
  • Signal Transduction*
  • Somites/metabolism
  • Trans-Activators*
  • Transcription Factors/metabolism
  • Zebrafish
PubMed
10642786 Full text @ Dev. Biol.
Abstract
The specification of different muscle cell types in the zebrafish embryo requires signals that emanate from the axial mesoderm. In previous studies we and others have shown that overexpression of different members of the Hedgehog protein family can induce the differentiation of two types of slow-twitch muscles, the superficially located slow-twitch fibres and the medially located muscle pioneer cells. Here we have investigated the requirement for Hedgehog signalling in the specification of these distinct muscle cell types in two ways: first, by characterising the effects on target gene expression and muscle cell differentiation of the u-type mutants, members of a phenotypic group previously implicated in Hedgehog signalling, and second, by analysing the effects of overexpression of the Patched1 protein, a negative regulator of Hedgehog signalling. Our results support the idea that most u-type genes are required for Hedgehog signalling and indicate that while such signalling is essential for slow myocyte differentiation, the loss of activity of one signal, Sonic hedgehog, can be partially compensated for by other Hedgehog family proteins.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping