PUBLICATION
Convergence and extension movements affect dynamic notochord-somite interactions essential for zebrafish slow muscle morphogenesis
- Authors
- Yin, C., and Solnica-Krezel, L.
- ID
- ZDB-PUB-070920-4
- Date
- 2007
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 236(10): 2742-2756 (Journal)
- Registered Authors
- Solnica-Krezel, Lilianna, Yin, Chunyue
- Keywords
- adaxial cell, knypek, trilobite, non-canonical Wnt, fibronectin, somitic boundary, gastrulation
- MeSH Terms
-
- Animals
- Body Patterning
- Cell Movement
- Embryonic Development
- Gene Expression Regulation, Developmental
- Hedgehog Proteins/metabolism
- Muscle Cells/cytology
- Muscle Cells/physiology*
- Muscle Development*
- Mutation
- Notochord/physiology*
- Somites/physiology*
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 17849437 Full text @ Dev. Dyn.
Citation
Yin, C., and Solnica-Krezel, L. (2007) Convergence and extension movements affect dynamic notochord-somite interactions essential for zebrafish slow muscle morphogenesis. Developmental Dynamics : an official publication of the American Association of Anatomists. 236(10):2742-2756.
Abstract
During vertebrate gastrulation, convergence and extension (C&E) movements shape and position the somites that form the fast and slow muscles. In zebrafish knypek;trilobite non-canonical Wnt mutants, defective C&E movements cause misshapen somites and reduction of slow muscle precursors, the adaxial cells. Here, we demonstrate essential roles of C&E in slow muscle morphogenesis. During segmentation, the adaxial cells change shapes and migrate laterally to form slow muscles at the myotome surface. Using confocal imaging techniques, we show that the adaxial cells undergo three-step shape changes, including dorsoventral elongation, anterior-ward rotation, and anteroposterior elongation. The adaxial cells in knypek;trilobite double mutants maintain prolonged contact with the notochord and fail to rotate anteriorly. Such a defect was suppressed by physical removal of their notochord or by introducing wild-type notochord cells into the mutant. We propose that in the double mutants, impaired C&E movements disrupt notochord development, which impedes the adaxial cell shape changes.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping