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Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions.

Xu X, Li WE, Huang GY, Meyer R, Chen T, Luo Y, Thomas MP, Radice GL, Lo CW - J. Cell Biol. (2001)

Bottom Line: Alternatively, Cx43alpha1 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 Cx43alpha1.Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43alpha1 deficiency.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Goddard Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.

ABSTRACT
Connexin 43 (Cx43alpha1) 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 Cx43alpha1 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 Cx43alpha1 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, Cx43alpha1 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 Cx43alpha1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43alpha1 deficiency. Based on these findings, we propose a model in which Cx43alpha1 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.

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Migratory paths of individual neural crest cells captured by time-lapse videomicroscopy. The color lines represent the migratory path of individual neural crest cells in a neural tube explant culture obtained with images captured every 10 min over 20 h. The circle represents the original position of each cell as it emerged from the neural tube explant. The migratory paths of neural crest cells derived from the N-cadherin–deficient embryo (right explant) are more tortuous than that of the wild-type embryo (left explant). Note that the neural tube explant flattened over time, thereby giving the erroneous impression that some of the neural crest cells originated from deep within the explant. Bar, 100 μm.
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fig3: Migratory paths of individual neural crest cells captured by time-lapse videomicroscopy. The color lines represent the migratory path of individual neural crest cells in a neural tube explant culture obtained with images captured every 10 min over 20 h. The circle represents the original position of each cell as it emerged from the neural tube explant. The migratory paths of neural crest cells derived from the N-cadherin–deficient embryo (right explant) are more tortuous than that of the wild-type embryo (left explant). Note that the neural tube explant flattened over time, thereby giving the erroneous impression that some of the neural crest cells originated from deep within the explant. Bar, 100 μm.

Mentions: To determine precisely how cell motility is affected by the loss of N-cadherin and how it may compare with cell motility perturbation elicited by Cx43α1 deficiency, we used time-lapse videomicroscopy and motion analysis to quantitate various cell motility parameters in individual neural crest cells. For this study, images of neural tube explant cultures were captured every 10 min over a 20-h interval. Examination of the resulting time-lapse movies revealed no discernible difference in the timing of neural crest cell emergence in explants derived from the N-cadherin– or Cx43α1-deficient mouse embryos compared with wild-type littermates. Tracking and analyzing the migratory paths of individual neural crest cells provided quantitative information on three cell motility parameters: speed, directionality (ratio of net over total distance traveled), and persistence of cell movement (direction change divided by speed). Surprisingly, this analysis showed that the speed of neural crest cell locomotion was elevated in the N-cadherin–deficient neural crest cells, but this was accompanied by a decrease in the directionality of cell movement (Table IV). This reduction in directionality is sufficiently large enough that it can be discerned visusally by the actual migratory paths of the individual neural crest cells (Fig. 3) . In addition, the persistence of cell movement was increased in the N-cadherin–deficient neural crest cells (Table IV; data not shown). A parallel analysis of Cx43α1-deficient neural crest cells revealed a similar reduction in the directionality of cell movement but no change in the speed or the persistence of cell movement (Table V). These results suggest that the altered cell motility of the N-cadherin–deficient neural crest cells is not simply due to the perturbation of Cx43α1-mediated gap junction communication.


Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions.

Xu X, Li WE, Huang GY, Meyer R, Chen T, Luo Y, Thomas MP, Radice GL, Lo CW - J. Cell Biol. (2001)

Migratory paths of individual neural crest cells captured by time-lapse videomicroscopy. The color lines represent the migratory path of individual neural crest cells in a neural tube explant culture obtained with images captured every 10 min over 20 h. The circle represents the original position of each cell as it emerged from the neural tube explant. The migratory paths of neural crest cells derived from the N-cadherin–deficient embryo (right explant) are more tortuous than that of the wild-type embryo (left explant). Note that the neural tube explant flattened over time, thereby giving the erroneous impression that some of the neural crest cells originated from deep within the explant. Bar, 100 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196865&req=5

fig3: Migratory paths of individual neural crest cells captured by time-lapse videomicroscopy. The color lines represent the migratory path of individual neural crest cells in a neural tube explant culture obtained with images captured every 10 min over 20 h. The circle represents the original position of each cell as it emerged from the neural tube explant. The migratory paths of neural crest cells derived from the N-cadherin–deficient embryo (right explant) are more tortuous than that of the wild-type embryo (left explant). Note that the neural tube explant flattened over time, thereby giving the erroneous impression that some of the neural crest cells originated from deep within the explant. Bar, 100 μm.
Mentions: To determine precisely how cell motility is affected by the loss of N-cadherin and how it may compare with cell motility perturbation elicited by Cx43α1 deficiency, we used time-lapse videomicroscopy and motion analysis to quantitate various cell motility parameters in individual neural crest cells. For this study, images of neural tube explant cultures were captured every 10 min over a 20-h interval. Examination of the resulting time-lapse movies revealed no discernible difference in the timing of neural crest cell emergence in explants derived from the N-cadherin– or Cx43α1-deficient mouse embryos compared with wild-type littermates. Tracking and analyzing the migratory paths of individual neural crest cells provided quantitative information on three cell motility parameters: speed, directionality (ratio of net over total distance traveled), and persistence of cell movement (direction change divided by speed). Surprisingly, this analysis showed that the speed of neural crest cell locomotion was elevated in the N-cadherin–deficient neural crest cells, but this was accompanied by a decrease in the directionality of cell movement (Table IV). This reduction in directionality is sufficiently large enough that it can be discerned visusally by the actual migratory paths of the individual neural crest cells (Fig. 3) . In addition, the persistence of cell movement was increased in the N-cadherin–deficient neural crest cells (Table IV; data not shown). A parallel analysis of Cx43α1-deficient neural crest cells revealed a similar reduction in the directionality of cell movement but no change in the speed or the persistence of cell movement (Table V). These results suggest that the altered cell motility of the N-cadherin–deficient neural crest cells is not simply due to the perturbation of Cx43α1-mediated gap junction communication.

Bottom Line: Alternatively, Cx43alpha1 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 Cx43alpha1.Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43alpha1 deficiency.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Goddard Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.

ABSTRACT
Connexin 43 (Cx43alpha1) 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 Cx43alpha1 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 Cx43alpha1 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, Cx43alpha1 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 Cx43alpha1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43alpha1 deficiency. Based on these findings, we propose a model in which Cx43alpha1 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.

Show MeSH
Related in: MedlinePlus