PUBLICATION

Hedgehog signalling is required for maintenance of myf5 and myoD expression and timely terminal differentiation in zebrafish adaxial myogenesis

Authors
Coutelle, O., Blagden, C.S., Hampson, R., Halai, C., Rigby, P.W.J., and Hughes, S.M.
ID
ZDB-PUB-010705-7
Date
2001
Source
Developmental Biology   236(1): 136-150 (Journal)
Registered Authors
Blagden, Chris, Hampson, Richard, Hughes, Simon M.
Keywords
skeletal muscle; zebrafish; myf5; myoD; hedgehog; differentiation; somite; myoblast; myogenesis
MeSH Terms
  • Myogenic Regulatory Factor 5
  • Zebrafish
  • In Situ Hybridization
  • In Situ Nick-End Labeling
  • Molecular Sequence Data
  • Sequence Homology, Amino Acid
  • Muscles/embryology
  • Cell Survival
  • Mutation
  • Cell Lineage
  • Immunohistochemistry
  • MyoD Protein/biosynthesis*
  • Animals
  • Time Factors
  • Up-Regulation
  • Proteins/metabolism*
  • Hedgehog Proteins
  • Trans-Activators*
  • Signal Transduction*
  • Cell Differentiation
  • Cloning, Molecular
  • DNA-Binding Proteins*
  • Notochord/metabolism
  • Amino Acid Sequence
  • Muscle Proteins/biosynthesis*
  • Phenotype
(all 26)
PubMed
11456450 Full text @ Dev. Biol.
Abstract
Hedgehog proteins have been implicated in the control of myogenesis in the medial vertebrate somite. In the mouse, normal epaxial expression of the myogenic transcription factor gene myf5 is dependent on Sonic hedgehog. Here we examine in zebrafish the interaction between Hedgehog signals, the expression of myoD family genes, including the newly cloned zebrafish myf5, and slow myogenesis. We show that Sonic hedgehog is necessary for normal expression of both myf5 and myoD in adaxial slow muscle precursors, but not in lateral paraxial mesoderm. Expression of both genes is initiated normally in rostral presomitic mesoderm in sonic you mutants, which lack all Sonic hedgehog. Similar initiation continues during tailbud outgrowth when the cells forming caudal somites are generated. However, adaxial cells in sonic you embryos are delayed in terminal differentiation and caudal adaxial cells fail to maintain myogenic regulatory factor expression. Despite these defects, other signals are able to maintain, or reinitiate, some slow muscle development in sonic you mutants. In the cyclops mutant, the absence of floorplate-derived Tiggywinkle hedgehog and Sonic hedgehog has no discernible effect on slow adaxial myogenesis. Similarly, the absence of notochord-derived Sonic hedgehog and Echidna hedgehog in mutants lacking notochord delays, but does not prevent, adaxial slow muscle development. In contrast, removal of both Sonic hedgehog and a floorplate signal, probably Tiggywinkle hedgehog, from the embryonic midline in cyclops;sonic you double mutants essentially abolishes slow myogenesis. We conclude that several midline signals, likely to be various Hedgehogs, collaborate to maintain adaxial slow myogenesis in the zebrafish embryo. Moreover, the data demonstrate that, in the absence of this required Hedgehog signalling, expression of myf5 and myoD is insufficient to commit cells to adaxial myogenesis.
Genes / Markers
Figures
Figure Gallery (6 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b16
    Deficiency
    b160
      Indel
      n1
        Small Deletion
        tbx392
          Point Mutation
          1 - 4 of 4
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          Human Disease / Model
          No data available
          Sequence Targeting Reagents
          No data available
          Fish
          Antibodies
          Name Type Antigen Genes Isotypes Host Organism
          Ab1-smyhcmonoclonal
            IgG2bMouse
            Ab-A4.1025monoclonal
              IgG2aMouse
              Ab-EB165monoclonal
                IgG1Mouse
                1 - 3 of 3
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                Orthology
                Gene Orthology
                myf5
                1 - 1 of 1
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                Engineered Foreign Genes
                No data available
                Mapping
                No data available