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Development of the nervous system depends on patterned neuronal migration and axonal growth, which are regulated by cell–cell and cell–substrate interactions (1). These interactions are mediated through cell adhesion molecules (CAMs), which include cadherins, selectins, integrins, mucins, and members of the IgG superfamily. Within the latter group are proteins, such as neural cell adhesion molecule, L1, and deleted in colon cancer (DCC), that are prominently expressed in the nervous system (2). In this issue of PNAS, investigators from the laboratory of Dr. Michael Charness (3) report findings that link these molecules to an important, preventable mental retardation syndrome. The role of CAMs in neural development has been established partly through the study of experiments of nature, spontaneous mutations in CAM genes that produce neurodevelopmental disorders in humans. The best example of such a gene is L1, which is located on human chromosome Xq28 and codes for a 143-kDa transmembrane glycoprotein containing six IgG-like and five fibronectin type III-like extracellular domains, a transmembrane segment, and a short cytoplasmic C terminus (Fig. 1). Signaling through L1 activates transduction pathways that involve inositol phosphates, mobilization of intracellular calcium, voltage-gated calcium influx, and cAMP (4–6). Activation of these pathways may underlie the effects of L1 in cell adhesion, neurite extension, neuronal migration, and axonal fasciculation (7). Inhibition of L1-mediated cell adhesion by ethanol and its antagonism by alcohols and peptides. The C terminus (C), intracytoplasmic region (IC), transmembrane segment (TM), fibronectin-like domains (FN), IgG-like domains (IgG), and N terminus (N) of L1 are shown. Ethanol interferes with the interaction between L1 and its homophilic or heterophilic binding partners (L1CAM binding …

Linking acquired neurodevelopmental disorders to defects in cell adhesion