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Cell behavior of wild‐type and myosin II loss of function neural crest cells in the zebrafish hindbrain during the epithelial to mesenchymal transition
Author(s) -
Halloran Mary C.,
Langenberg Tobias,
Berndt Jason D.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a80-a
Subject(s) - neural crest , filopodia , zebrafish , hindbrain , microbiology and biotechnology , biology , cell migration , epithelial–mesenchymal transition , morphogenesis , myosin , motility , live cell imaging , focal adhesion , actin , cell , cancer , signal transduction , metastasis , embryo , genetics , gene
The proper induction and migration of neural crest cells (NCCs) is essential to the appropriate development of craniofacial structures and the peripheral nervous system. A critical step in NCC development is the epithelial to mesenchymal transition (EMT) they must undergo to delaminate from the neuroepithelium and initiate migration. EMT is a prevalent phenomenon in tissue morphogenesis during development and in cancer progression. The EMT involves dramatic changes in cell adhesion, the cytoskeleton, and cell behavior. However, little is known about the mechanisms regulating cell motility changes, or about the specific changes in behavior of NCCs undergoing the EMT in vivo. We have used time‐lapse imaging of NCCs in the zebrafish hindbrain to show that NCCs display characteristic changes in cell adhesion and extend specific types of protrusions during EMT. We find that blebbing protrusive activity precedes filopodial extension and the onset of migration. Using live imaging of actin dynamics, we show that actin is localized differently in blebs versus filopodia. Moreover, we find that blebbing depends on the activity of myosin II and disruption of Rho‐kinase or myosin II activity leads to defects in NCC migration. Our characterization of the detailed cell behaviors during EMT provides a basis for further experiments to understand the molecular mechanisms regulating EMT.