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ZFIN ID: ZDB-PUB-991216-1
Control of muscle cell-type specification in the zebrafish embryo by hedgehog signalling
Lewis, K.E., Currie, P.D., Roy, S., Schauerte, H., Haffter, P., and Ingham, P.W.
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.
FIGURES
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.
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