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.
Wong and Reiter have explored the possibility that hair follicle stem cells can give rise to basal cell carcinoma (BCC). They expressed in mice an inducible human BCC-derived oncogenic allele of Smoothened, SmoM2, under the control of either the cytokeratin 14 (K14) or cytokeratin 15 (K15) promoter. Smoothened encodes a G-protein-coupled receptor protein in the hedgehog pathway, the misregulation of which is implicated in BCC and other human cancers. Chronic injury is thought to be a contributing factor. The authors used K14 as a marker for stem cells in the basal layer of the epidermis and K15 as a marker for epidermal stem cells in the bulge of hair follicles. Upon activation, K14 construct-bearing mice readily formed BCC-like tumours, whereas this was not the case in K15:SmoM2-carrying mice. Upon wounding the epidermis, however, there was widespread BCC-like tumour formation in the skin of K15:SmoM2 mice. The authors conclude that wounding recruited bulge epidermal stem cells to the surface, allowing the cells to escape quiescence in the stem cell niche and to arrive in an environment where the hedgehog pathway becomes activated and therefore tumorigenesis is elicited. While this is a provocative result and the authors' conclusion may well be correct, there are alternative explanations.
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