Effects of antibodies against N-cadherin and N-CAM on the cranial neural crest and neural tube

Bronner‐Fraser, Marianne; Wolf, John J.; Murray, Ben A.

doi:10.1016/0012-1606(92)90114-v

Cited by 176 publications

(85 citation statements)

References 36 publications

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“…In agreement with previous studies, we found that Ncadherin was expressed by neural crest cells as they coalesced to form sympathetic ganglia (Fig. 1C,F) (Bronner-Fraser et al, 1992;Pla et al, 2001). To test N-cadherin function during sympathetic ganglion formation, embryos that had previously been injected with EGFP at HH St. 10 to label premigratory neural crest cells were injected with the blocking N-cadherin antibody, NCD2, in ovo at HH St. 17.…”

Section: N-cadherin Is Expressed By Neural Crest Cells Segregating Insupporting

confidence: 91%

“…Based on extensive evidence for cadherin regulation as a mechanism that mediates cell aggregation in embryogenesis (Radice et al, 1997;Linask et al, 1998;Bronner-Fraser et al, 1992;Nieto, 2001;Pla et al, 2001), we re-examined the timing of N-cadherin expression in the trunk of E2.5-3.5 chick embryos during sympathetic ganglia formation. In agreement with previous studies, we found that Ncadherin was expressed by neural crest cells as they coalesced to form sympathetic ganglia (Fig.…”

Section: N-cadherin Is Expressed By Neural Crest Cells Segregating Inmentioning

confidence: 99%

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Eph/ephrins and N-cadherin coordinate to control the pattern of sympathetic ganglia

et al. 2006

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Previous studies have suggested that the segmental pattern of neural-crest-derived sympathetic ganglia arises as a direct result of signals that restrict neural crest cell migratory streams through rostral somite halves. We recently showed that the spatiotemporal pattern of chick sympathetic ganglia formation is a two-phase process. Neural crest cells migrate laterally to the dorsal aorta, then surprisingly spread out in the longitudinal direction, before sorting into discrete ganglia. Here, we investigate the function of two families of molecules that are thought to regulate cell sorting and aggregation. By blocking Eph/ephrins or N-cadherin function, we measure changes in neural crest cell migratory behaviors that lead to alterations in sympathetic ganglia formation using a recently developed sagittal slice explant culture and 3D confocal time-lapse imaging. Our results demonstrate that local inhibitory interactions within inter-ganglionic regions, mediated by Eph/ephrins, and adhesive cell-cell contacts at ganglia sites, mediated by N-cadherin, coordinate to sculpt discrete sympathetic ganglia.

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Section: N-cadherin Is Expressed By Neural Crest Cells Segregating Insupporting

confidence: 91%

Section: N-cadherin Is Expressed By Neural Crest Cells Segregating Inmentioning

confidence: 99%

Eph/ephrins and N-cadherin coordinate to control the pattern of sympathetic ganglia

et al. 2006

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“…This E-to Ncadherin switch during neurulation has often been interpreted as an event necessary both for the acquisition of the morphological features of neural epithelial cells and for the movements of neurulation to occur. However, despite a variety of experiments in different animal models that uncovered the importance of N-cadherin in early neural development (Bronner-Fraser et al, 1992;Radice et al, 1997;Lele et al, 2002;Hong and Brewster, 2006;Nandadasa et al, 2009), these hypotheses have never been tested experimentally, and the biological significance of the change in cadherin expression during neurulation remains, therefore, unclear. In particular, it is not known why, contrary to epithelial cell lines established in vitro, E-cadherin loss in the neural epithelium does not provoke EMT.…”

Section: Introductionmentioning

confidence: 99%

Timing and kinetics of E‐ to N‐cadherin switch during neurulation in the avian embryo

Dady

Blavet

Duband

2012

Developmental Dynamics

107

132

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Background: During embryonic development, cadherin switches are correlated with tissue remodelings, such as epithelium-to-mesenchyme transition (EMT). An E-to N-cadherin switch also occurs during neurogenesis, but this is not accompanied with EMT. The biological significance of this switch is currently unknown. Results: We analyzed the timing and kinetics of the E-to N-cadherin switch during early neural induction and neurulation in the chick embryo, in relation to the patterns of their transcriptional regulators. We found that deployment of the E-to N-cadherin switch program varies considerably along the embryonic axis. Rostrally in regions of primary neurulation, it occurs progressively both in time and space in a manner that appears neither in connection with morphological transformation of neural epithelial cells nor in synchrony with movements of neurulation. Caudally, in regions of secondary neurulation, neurogenesis was not associated with cadherin switch as N-cadherin pre-existed before formation of the neural tube. We also found that, during neural development, cadherin switch is orchestrated by a set of transcriptional regulators distinct from those involved in EMT. Conclusions: Our results indicate that cadherin switch correlates with the partition of the neurectoderm into its three main populations: ectoderm, neural crest, and neural tube.

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“…A number of molecules are known to participate in neural crest delamination and migration, such as cadherins, Rho GTPases, Noggin and several extracellular matrix molecules (Borchers et al, 2001;Bronner-Fraser et al, 1992;Henderson et al, 2000;Hoffmann and Balling, 1995;Kimura et al, 1995;Liu and Jessell, 1998;Nakagawa and Takeichi, 1995;Nakagawa and Takeichi, 1998;Perris and Perissinotto, 2000;Pla et al, 2001;Sela-Donenfeld and Kalcheim, 1999;Sela-Donenfeld and Kalcheim, 2000;Takeichi et al, 2000;Vallin et al, 1998; Van de Putte et al, 2003;Yagi and Takeichi, 2000). However, the mechanisms by which extracellular signals are integrated with cell adhesion and cytoskeletal modification to orchestrate the cell movements underlying delamination and movement of the neural crest are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Essential role of non-canonical Wnt signalling in neural crest migration

et al. 2005

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Migration of neural crest cells is an elaborate process that requires the delamination of cells from an epithelium and cell movement into an extracellular matrix. In this work, it is shown for the first time that the non-canonical Wnt signalling [planar cell polarity (PCP) or Wnt-Ca2+] pathway controls migration of neural crest cells. By using specific Dsh mutants, we show that the canonical Wnt signalling pathway is needed for neural crest induction, while the non-canonical Wnt pathway is required for neural crest migration. Grafts of neural crest tissue expressing non-canonical Dsh mutants, as well as neural crest cultured in vitro, indicate that the PCP pathway works in a cell-autonomous manner to control neural crest migration. Expression analysis of non-canonical Wnt ligands and their putative receptors show that Wnt11 is expressed in tissue adjacent to neural crest cells expressing the Wnt receptor Frizzled7 (Fz7). Furthermore, loss- and gain-of-function experiments reveal that Wnt11 plays an essential role in neural crest migration. Inhibition of neural crest migration by blocking Wnt11 activity can be rescued by intracellular activation of the non-canonical Wnt pathway. When Wnt11 is expressed opposite its normal site of expression, neural crest migration is blocked. Finally, time-lapse analysis of cell movement and cell protrusion in neural crest cultured in vitro shows that the PCP or Wnt-Ca2+ pathway directs the formation of lamellipodia and filopodia in the neural crest cells that are required for their delamination and/or migration.

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Effects of antibodies against N-cadherin and N-CAM on the cranial neural crest and neural tube

Cited by 176 publications

References 36 publications

Eph/ephrins and N-cadherin coordinate to control the pattern of sympathetic ganglia

Eph/ephrins and N-cadherin coordinate to control the pattern of sympathetic ganglia

Timing and kinetics of E‐ to N‐cadherin switch during neurulation in the avian embryo

Essential role of non-canonical Wnt signalling in neural crest migration

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