INITIAL STEPS OF MYOGENESIS IN SOMITES ARE INDEPENDENT OF INFLUENCE FROM AXIAL STRUCTURES

Citation
E. Bober et al., INITIAL STEPS OF MYOGENESIS IN SOMITES ARE INDEPENDENT OF INFLUENCE FROM AXIAL STRUCTURES, Development, 120(11), 1994, pp. 3073-3082
Citations number
43
Categorie Soggetti
Developmental Biology
Journal title
ISSN journal
09501991
Volume
120
Issue
11
Year of publication
1994
Pages
3073 - 3082
Database
ISI
SICI code
0950-1991(1994)120:11<3073:ISOMIS>2.0.ZU;2-R
Abstract
Formation of paraxial muscles in vertebrate embryos depends upon inter actions between early somites and the neural tube and notochord, Remov al of both axial structures results in a complete loss of epaxial myot omal muscle, whereas hypaxial and limb muscles develop normally. We re port that chicken embryos, after surgical removal of the neural tube a t the level of the unsegmented paraxial mesoderm, start to develop myo tomal cells that express transcripts for the muscle-specific regulator s MyoD and myogenin. These cells also make desmin, indicating that the initial steps of axial skeletal muscle formation tan occur in the abs ence of the neural tube, However, a few days following the extirpation , the expression of MyoD and myogenin transcripts gradually disappears , and becomes almost undetectable after 4 days, From these observation s we conclude that the neural tube is not required for the generation of the skeletal muscle cell lineage, but may support the survival or m aitenance of further differentiation of the myotomal cell compartment. Notochord transplanted medially or laterally to the unsegmented parax ial mesoderm leads to a ventralization of axial structures but does no t entirely prevent the early appearance of myoblasts expressing MyoD t ranscripts, However, the additional notochord inhibits subsequent deve lopment and maturation of myotomes. Taken together, our data suggest t hat neural tube promotes, and notochord inhibits, the process of myoge nesis in axial muscles at a developmental step following the initial e xpression of myogenic bHLH regulators.