Shaping the zebrafish notochord
- Glickman, N.S., Kimmel, C.B., Jones, M.A., and Adams, R.J.
- Development (Cambridge, England) 130(5): 873-887 (Journal)
- Registered Authors
- Adams, Richard, Holtzman, Nathalia Glickman, Kimmel, Charles B.
- MeSH Terms
- Cell Differentiation/physiology
- Cell Movement/physiology*
- Cell Size
- Fetal Proteins
- Fluorescent Dyes/metabolism
- Microscopy, Confocal
- Models, Biological
- Notochord/growth & development
- T-Box Domain Proteins/genetics
- T-Box Domain Proteins/metabolism
- Time Factors
- Zebrafish/anatomy & histology
- Zebrafish/growth & development
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- 12538515 Full text @ Development
Glickman, N.S., Kimmel, C.B., Jones, M.A., and Adams, R.J. (2003) Shaping the zebrafish notochord. Development (Cambridge, England). 130(5):873-887.
Promptly after the notochord domain is specified in the vertebrate dorsal mesoderm, it undergoes dramatic morphogenesis. Beginning during gastrulation, convergence and extension movements change a squat cellular array into a narrow, elongated one that defines the primary axis of the embryo. Convergence and extension might be coupled by a highly organized cellular intermixing known as mediolateral intercalation behavior (MIB). To learn whether MIB drives early morphogenesis of the zebrafish notochord, we made 4D recordings and quantitatively analyzed both local cellular interactions and global changes in the shape of the dorsal mesodermal field. We show that MIB appears to mediate convergence and can account for extension throughout the dorsal mesoderm. Comparing the notochord and adjacent somitic mesoderm reveals that extension can be regulated separately from convergence. Moreover, mutational analysis shows that extension does not require convergence. Hence, a cellular machine separate from MIB that can drive dorsal mesodermal extension exists in the zebrafish gastrula. The likely redundant control of morphogenesis may provide for plasticity at this critical stage of early development.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes