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The tight junction protein cingulin modulates chick neural crest cell emigration
Author(s) -
Taneyhill Lisa Anne,
Wu ChyongYi,
Jhingory Sharon
Publication year - 2011
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.25.1_supplement.180.2
Subject(s) - neural crest , neural fold , neuroepithelial cell , microbiology and biotechnology , neural tube , biology , neural plate , neural stem cell , stem cell , embryo
The neural crest gives rise to a diverse range of cell types in the developing vertebrate embryo. Initially existing as adherent epithelial cells (the premigratory neural crest), these cells undergo an epithelial‐to‐mesenchymal transition (EMT) characterized by a loss of intercellular contacts to facilitate their emigration from the dorsal neural tube. We have previously shown that components of premigratory neural crest cell adherens junctions must be properly regulated for appropriate neural crest cell migration. We now demonstrate that the tight junction protein cingulin plays a critical role in controlling neural crest cell emigration. Prior to EMT, cingulin is expressed apically throughout the chick midbrain neuroepithelium. As neural crest cells delaminate, cingulin is diminished dorsally, and emerging neural crest cells lack cingulin. Depletion of cingulin leads to premature neural crest cell emigration, whereas overexpression of cingulin induces ectopic breakdown of the basal lamina in ventrolateral neuroepithelial cells and the inappropriate movement of neuroepithelial and neural crest cells. These latter results correlate with changes in the levels of neural tube Rho GTPases. Taken together, these data reveal a novel function for cingulin in regulating neural crest cell emigration during vertebrate development. This research is supported by the NIH (R00HD055034) and NSF (IOS‐0948525).