scholarly journals Lectin binding to neural crest cells. Changes of the cell surface during differentiation in vitro.

1978 ◽  
Vol 76 (3) ◽  
pp. 628-638 ◽  
Author(s):  
M Sieber-Blum ◽  
A M Cohen
Keyword(s):  
Cell Surface ◽  
Neural Crest ◽  
Lectin Binding ◽  
Neural Crest Cells ◽  
Nerve Fibers ◽  
Con A ◽  
Contact Points ◽  
Cell Processes ◽  
Surface Carbohydrates

To examine possible changes in cell surface carbohydrates, fluorescent lectins were applied at various times during differentiation of neural crest cells in vitro. The pattern and intensity of binding of several lectins changed as the crest cells developed into melanocytes and adrenergic cells. Considerable amounts of concanavalin A (Con A) and wheat germ agglutinin (WGA) bound to all unpigmented cells throughout the culture period. Melanocytes, however, bound much less of these lectins. Soy bean agglutinin (SBA), unlike Con A and WGA, only bound later in development to unpigmented cells at about the time when catecholamines were detected histochemically. Binding of SBA could be induced in younger cultures by pretreating the cells with neuraminidase. Melanocytes, however, did not bind detectable amounts of SBA even if treated with neuraminidase. The SBA-binding sites were often concentrated on cytoplasmic extensions and on contact points between neighboring cells, even when receptor mobility was restricted by prefixation of the cells or adsorption of lectin at 0 degrees C. All three lectins bound to cell processes resembling nerve fibers in particularly high amounts.

scholarly journals Evidence for a novel enzymatic mechanism of neural crest cell migration on extracellular glycoconjugate matrices.

1986 ◽  
Vol 102 (2) ◽  
pp. 432-441 ◽  
Author(s):  
R B Runyan ◽  
G D Maxwell ◽  
B D Shur
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Neural Crest ◽  
Basal Lamina ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Crest Cell Migration ◽  
Dose Dependent ◽  
Crest Cell

Migrating embryonic cells have high levels of cell surface galactosyltransferase (GalTase) activity. It has been proposed that GalTase participates during migration by recognizing and binding to terminal N-acetylglucosamine (GlcNAc) residues on glycoconjugates within the extracellular matrix (Shur, B. D., 1982, Dev. Biol. 91:149-162). We tested this hypothesis using migrating neural crest cells as an in vitro model system. Cell surface GalTase activity was perturbed using three independent sets of reagents, and the effects on cell migration were analyzed by time-lapse microphotography. The GalTase modifier protein, alpha-lactalbumin (alpha-LA), was used to inhibit surface GalTase binding to terminal GlcNAc residues in the underlying substrate. alpha-LA inhibited neural crest cell migration on basal lamina-like matrices in a dose-dependent manner, while under identical conditions, alpha-LA had no effect on cell migration on fibronectin. Control proteins, such as lysozyme (structurally homologous to alpha-LA) and bovine serum albumin, did not effect migration on either matrix. Second, the addition of competitive GalTase substrates significantly inhibited neural crest cell migration on basal lamina-like matrices, but as above, had no effect on migration on fibronectin. Comparable concentrations of inappropriate sugars also had no effect on cell migration. Third, addition of the GalTase catalytic substrate, UDPgalactose, produced a dose-dependent increase in the rate of cell migration. Under identical conditions, the inappropriate sugar nucleotide, UDPglucose, had no effect. Quantitative enzyme assays confirmed the presence of GalTase substrates in basal lamina matrices, their absence in fibronectin matrices, and the ability of alpha-LA to inhibit GalTase activity towards basal lamina substrates. Laminin was found to be a principle GalTase substrate in the basal lamina, and when tested in vitro, alpha-LA inhibited cell migration on laminin. Together, these experiments show that neural crest cells have at least two distinct mechanisms for interacting with the substrate during migration, one that is fibronectin-dependent and one that uses GalTase recognition of basal lamina glycoconjugates.

Effects of vitamin A on the behaviour of migratory neural crest cells in vitro

1982 ◽  
Vol 57 (1) ◽  
pp. 331-350 ◽  
Author(s):  
P. Thorogood ◽  
L. Smith ◽  
A. Nicol ◽  
R. McGinty ◽  
D. Garrod
Keyword(s):  
Cell Surface ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Initial Exposure ◽  
Normal Medium ◽  
Locomotory Behaviour ◽  
Cranial Neural Crest Cells ◽  
In Vivo Effects

It has been proposed elsewhere that the teratogenic effects of retinoids on craniofacial morphogenesis are caused by a disturbance of the migration of cranial neural crest cells. The effects of 3.5 X 10(−5) M and 3.5 X 10(−6) M-retinol on the migration of avian neural crest cells in vitro have been investigated by monitoring cell morphology, locomotory behaviour, fibronectin distribution and actin-microfilament organization. Retinol retards migration by affecting cell-to-substratum adhesiveness. Cells exposed to medium containing retinol are less adherent to the substratum, and although the cell surface is very mobile, are unable to extend or maintain lamellipodia. As a consequence the cells do not actively translocate. Fibronectin distribution at the cell surface is sparse, possibly as a result of shedding, and actin distribution remains diffuse. At the retinol molarities used all these effects are reversible. Thus cells allowed to recover in normal medium flatten out, display lamellipodia and commence active translocation. Fibronectin becomes organized into a fibrillar array and actin microfilaments become organized into cables. The period needed for this recovery is directly related to the molarity of retinol during the initial exposure; after recovery the retinol-treated cells are virtually indistinguishable from control cells. We propose that in vivo the effects of retinoids might be to impair cell-extracellular matrix interaction, thus impeding a cell's ability to migrate through that matrix. Contrary to previous suggestions, the in vivo effects are probably not in any way ‘specific’ to neural crest cells but are more accurately considered as ‘selective’, in that any cell undergoing migration would be similarly affected.

Induction of melanocyte precursors from neural crest cells surrounding the neural tube-like structures developed in vitro using mouse ES cell culture

2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  
Keyword(s):  
Cell Culture ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Es Cell ◽  
Mouse Es Cell

Cellular fibronectin promotes adrenergic differentiation of quail neural crest cells in vitro

1981 ◽  
Vol 133 (2) ◽  
pp. 285-295 ◽  
Author(s):  
Maya Sieber-Blum ◽  
Fritz Sieber ◽  
Kenneth M. Yamada
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Cellular Fibronectin

scholarly journals Lineage-specific requirements of β-catenin in neural crest development

2002 ◽  
Vol 159 (5) ◽  
pp. 867-880 ◽  
Author(s):  
Lisette Hari ◽  
Véronique Brault ◽  
Maurice Kléber ◽  
Hye-Youn Lee ◽  
Fabian Ille ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Neural Crest Stem Cells ◽  
Downstream Signaling ◽  
Neural Crest Development ◽  
Sensory Neurogenesis

β-Catenin plays a pivotal role in cadherin-mediated cell adhesion. Moreover, it is a downstream signaling component of Wnt that controls multiple developmental processes such as cell proliferation, apoptosis, and fate decisions. To study the role of β-catenin in neural crest development, we used the Cre/loxP system to ablate β-catenin specifically in neural crest stem cells. Although several neural crest–derived structures develop normally, mutant animals lack melanocytes and dorsal root ganglia (DRG). In vivo and in vitro analyses revealed that mutant neural crest cells emigrate but fail to generate an early wave of sensory neurogenesis that is normally marked by the transcription factor neurogenin (ngn) 2. This indicates a role of β-catenin in premigratory or early migratory neural crest and points to heterogeneity of neural crest cells at the earliest stages of crest development. In addition, migratory neural crest cells lateral to the neural tube do not aggregate to form DRG and are unable to produce a later wave of sensory neurogenesis usually marked by the transcription factor ngn1. We propose that the requirement of β-catenin for the specification of melanocytes and sensory neuronal lineages reflects roles of β-catenin both in Wnt signaling and in mediating cell–cell interactions.

scholarly journals Stimulation of corneal differentiation by interaction between cell surface and extracellular matrix. I. Morphometric analysis of transfilter "induction".

1975 ◽  
Vol 66 (2) ◽  
pp. 275-291 ◽  
Author(s):  
L Meier ◽  
E D Hay
Keyword(s):  
Extracellular Matrix ◽  
Electron Microscope ◽  
Cell Surface ◽  
Pore Size ◽  
Collagen Synthesis ◽  
Lens Capsule ◽  
Physical Contact ◽  
Corneal Epithelial ◽  
Cell Processes

The present study was undertaken to determine whether or not physical contact with the substratum is essential for the stimulatory effect of extracellular matrix (ECM) on corneal epithelial collagen synthesis. Previous studies showed that collagenous substrata stimulate isolated epithelia to produce three times as much collagen as they produce on noncollagenous substrate; killed collagenous substrata (e.g., lens capsule) are just as effective as living substrata (e.g., living lens) in promoting the production of new corneal stroma in vitro. In the experiments to be reported here, corneal epithelia were placed on one side of Nucleopore filters of different pore sizes and killed lens capsule on the other, with the expectation that contact of the reacting cells with the lens ECM should be limited by the number and size of the cell processes that can tranverse the pores. Transfilter cultures were grown for 24 h in [3H]proline-containing median and incorporation of isotope into hot trichloroacetic acid-soluble protein was used to measure corneal epithelial collagen production. Epithelial collagen synthesis increases directly as the size of the pores in the interposed filter increases and decreases as the thickness of the filter layer increases. Cell processes within Nucleopore filters were identified with the transmission electron microscope with difficulty; with the scanning electron microscope, however, the processes could easily be seen emerging from the undersurface of even 0.1-mum pore size filters. Morphometric techniques were used to show that cell surface area thus exposed to the underlying ECM is linearly correlated with enhancement of collagen synthesis. Epithelial cell processes did not pass through ultrathin (25-mum thick) 0.45-mum pore size Millipore filters nor did "induction" occur across them. The results are discussed in relation to current theories of embryonic tissue interaction.

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