PUBLICATION
Rho-kinase and myosin II affect dynamic neural crest cell behaviors during epithelial to mesenchymal transition in vivo
- Authors
- Berndt, J.D., Clay, M.R., Langenberg, T., and Halloran, M.C.
- ID
- ZDB-PUB-081022-32
- Date
- 2008
- Source
- Developmental Biology 324(2): 236-244 (Journal)
- Registered Authors
- Berndt, Jason, Halloran, Mary, Langenberg, Tobias
- Keywords
- neural crest, zebrafish, myosin II, Rho-kinase, blebbing
- MeSH Terms
-
- Actins/metabolism
- Neural Crest/embryology*
- Neural Crest/ultrastructure
- Pseudopodia/physiology
- Cell Membrane/metabolism
- Animals, Genetically Modified/embryology
- Animals, Genetically Modified/metabolism
- Mesoderm/embryology
- Cytokinesis
- Cell Adhesion
- Epithelium/embryology
- Cell Differentiation*
- Zebrafish Proteins/metabolism
- rho-Associated Kinases/metabolism*
- Animals
- Cell Movement
- Zebrafish/embryology*
- Zebrafish/metabolism
- Rhombencephalon/embryology
- Myosin Type II/metabolism*
- PubMed
- 18926812 Full text @ Dev. Biol.
Citation
Berndt, J.D., Clay, M.R., Langenberg, T., and Halloran, M.C. (2008) Rho-kinase and myosin II affect dynamic neural crest cell behaviors during epithelial to mesenchymal transition in vivo. Developmental Biology. 324(2):236-244.
Abstract
The induction and migration of neural crest cells (NCCs) is essential to the development of craniofacial structures and the peripheral nervous system. A critical step in the development of NCCs is the epithelial to mesenchymal transition (EMT) that they undergo in order to initiate migration. Several transcription factors are important for the NCC EMT. However, less is known about the effectors regulating changes in cell adhesion, the cytoskeleton, and cell motility associated with the EMT or about specific changes in the behavior of cells undergoing EMT in vivo. We used time-lapse imaging of NCCs in the zebrafish hindbrain to show that NCCs undergo a stereotypical series of behaviors during EMT. We find that loss of cell adhesion and membrane blebbing precede filopodial extension and the onset of migration. Live imaging of actin dynamics shows that actin localizes differently in blebs and filopodia. Moreover, we find that disruption of myosin II or Rho-kinase (ROCK) activity inhibits NCC blebbing and causes reduced NCC EMT. These data reveal roles for myosin II and ROCK in NCC EMT in vivo, and provide a detailed characterization of NCC behavior during EMT that will form a basis for further mechanistic studies.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping