scholarly journals N-Cadherin and Cx43α1 Gap Junctions Modulates Mouse Neural Crest Cell Motility via Distinct Pathways

2001 ◽  
Vol 8 (4-6) ◽  
pp. 321-324 ◽  
Author(s):  
X. Xu ◽  
W. E. I. Li ◽  
G. Y. Huang ◽  
R. Meyer ◽  
T. Chen ◽  
...  
2001 ◽  
Vol 154 (1) ◽  
pp. 217-230 ◽  
Author(s):  
X. Xu ◽  
W.E.I. Li ◽  
G.Y. Huang ◽  
R. Meyer ◽  
T. Chen ◽  
...  

Connexin 43 (Cx43α1) gap junction has been shown to have an essential role in mediating functional coupling of neural crest cells and in modulating neural crest cell migration. Here, we showed that N-cadherin and wnt1 are required for efficient dye coupling but not for the expression of Cx43α1 gap junctions in neural crest cells. Cell motility was found to be altered in the N-cadherin–deficient neural crest cells, but the alterations were different from that elicited by Cx43α1 deficiency. In contrast, wnt1-deficient neural crest cells showed no discernible change in cell motility. These observations suggest that dye coupling may not be a good measure of gap junction communication relevant to motility. Alternatively, Cx43α1 may serve a novel function in motility. We observed that p120 catenin (p120ctn), an Armadillo protein known to modulate cell motility, is colocalized not only with N-cadherin but also with Cx43α1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43α1 deficiency. Based on these findings, we propose a model in which Cx43α1 and N-cadherin may modulate neural crest cell motility by engaging in a dynamic cross-talk with the cell's locomotory apparatus through p120ctn signaling.


2002 ◽  
Vol 16 (6) ◽  
pp. 825-839 ◽  
Author(s):  
Leah C Fuller ◽  
Shannon K Cornelius ◽  
Charles W Murphy ◽  
Darrell J Wiens

2019 ◽  
Author(s):  
Karyn Jourdeuil ◽  
Lisa A. Taneyhill

ABSTRACTGap junctions are intercellular channels that allow for the diffusion of small ions and solutes between coupled cells. Connexin 43 (Cx43), also known as Gap Junction Protein α1, is the most broadly expressed gap junction protein in vertebrate development. Cx43 is strongly expressed in premigratory cranial neural crest cells and is maintained throughout the neural crest cell epithelial-to-mesenchymal transition (EMT), but its function in these cells is not known. To this end, we have used a combination of in vivo and ex vivo live imaging with confocal microscopy, immunohistochemistry, and functional assays to assess gap junction formation, and Cx43 function, in chick premigratory cranial neural crest cells. Our results demonstrate that gap junctions exist between chick premigratory and migratory cranial neural crest cells, with Cx43 depletion inhibiting the function of gap junctions. While a reduction in Cx43 levels just prior to neural crest cell EMT did not affect EMT and subsequent emigration of neural crest cells from the neural tube, the size of the premigratory neural crest cell domain was decreased in the absence of any changes in cell proliferation or death. Collectively, these data identify a role for Cx43 within the chick premigratory cranial neural crest cell population prior to EMT and migration.


1983 ◽  
Vol 61 (1) ◽  
pp. 299-323
Author(s):  
C.A. Erickson ◽  
E.A. Turley

Extracellular matrix components such as collagen, fibronectin and sulphated glycosaminoglycans can act as substrata that promote neural crest motility in vitro, in the absence of serum. The cells appear to be less adhesive and move more randomly on collagen or chondroitin sulphate substrata than on fibronectin substrata. Cells do not spread or become motile on plastic dishes to which hyaluronate has been bound, presumably owing to weak adhesion to this surface. Hyaluronate added to the medium alone has little effect on cell motility. When combinations of matrix molecules are used as substrata, however, the presence of fibronectin increases spreading, directional persistence of cell motility and speed of movement above that observed on collagen alone. When added to fibronectin, chondroitin sulphate appears to reduce adhesions slightly, since the cells are more rounded. Hyaluronate added in the medium significantly reduces the extent, speed and directionality of movement on fibronectin substrata. The presence of collagen in combination with fibronectin plus glycosaminoglycans does not have a noticeable effect on cell motile behaviour, beyond that observed with fibronectin alone. The effects of combinations of matrix compounds on neural crest cell motility are thus predictable, and can be explained in terms of the known adhesive properties and reported binding interactions of these molecules. These studies in vitro are compared with neural crest cell motility in vivo.


2021 ◽  
Author(s):  
Elizabeth A. Bearce ◽  
Benjamin Pratt ◽  
Erin Rutherford ◽  
Leslie Carandang ◽  
Laura Anne Lowery

AbstractCoordinated cell migration is critical during embryogenesis, as cells must leave their point of origin, navigate a complex barrage of signals, and accurately position themselves to facilitate correct tissue and organ formation. The cell motility process relies on dynamic interactions of the F-actin and microtubule (MT) cytoskeletons. Our work focuses on how one MT plus-end regulator, Transforming Acidic Coiled-Coil 3 (Tacc3), can impact migration of cranial neural crest cells in Xenopus laevis. We previously demonstrated that tacc3 expression is expressed in cranial neural crest cells, and that Tacc3 can function as a MT plus-end tracking protein to regulate MT growth velocities. Here, we demonstrate that manipulation of Tacc3 protein levels is sufficient to alter cranial neural crest cell velocity in vitro. Tacc3 overexpression drives increased single-cell migration velocities, while Tacc3 KD results in reduced cell velocity and defective explant dispersion. We also show that Tacc3 can have spatially-enhanced effects on MT plus-end growth velocities as well as effects on focal adhesion remodeling. Together, we demonstrate that Tacc3 can facilitate neural crest cell motility through spatially-enhanced cytoskeletal remodeling, which may underlie the enhanced metastatic potential of Tacc3-overexpressing tumor cells.


1997 ◽  
Vol 233 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Alice Beauvais-Jouneau ◽  
Annie Delouvée ◽  
Susan E. Craig ◽  
Martin J. Humphries ◽  
Jean-Paul Thiery ◽  
...  

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