Regulation of axonal growth in the vertebrate nervous system by interactions between glycoproteins belonging to two subgroups of the immunoglobulin superfamily.

Sonderegger, P.; Rathjen, Fritz G.

doi:10.1083/jcb.119.6.1387

Cited by 152 publications

(92 citation statements)

References 97 publications

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“…The neural cell adhesion molecule L1 in the mouse [Ng-CAM, 8D9 or G4 as possible homologs in the chicken (Lagenaur and Lemmon 1987;Grumet 1992;Sonderegger and Rathjen 1992)] is an integral cell surface glycoprotein (Rathjen and Schachner 1984;Faissner et al 1985) and was originally defined as an adhesion molecule because antibodies against it inhibited cell adhesion and aggregation . Lemmon et al (1989) showed that antibodies to chicken and mouse L1 block neurite outgrowth from mouse neurons, thus confirming that mouse and chicken L1 interact homophilically.…”

Section: Introductionmentioning

confidence: 99%

A role for a chicken homolog of the neural cell adhesion molecule L1 in consolidation of memory for a passive avoidance task in the chick.

Scholey¹,

Mileusnic²,

Schachner³

et al. 1995

Learn. Mem.

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Intracranial injection of antibodies directed against the neural cell adhesion molecule L1 resulted in amnesia for passive avoidance training in day-old chicks tested 24 hr subsequently. L1 antibodies were amnesic when administered at one of two time windows: 30 min pretraining and 5.5-8 hr post-training. No amnesia was apparent if injections were made at times before, between, or after these time windows (-2, +1, +3, +4, or +12 hr relative to training). A fragment of the L1 molecule derived from the external fibronectin domains FN1-5 produced amnesia only when injected at the 5.5-hr timepoint, whereas a fragment of the immunoglubin-like domains Ig I-VI produced amnesia only when injected 30 min prior to training. We have shown previously that long-term memory for the passive avoidance task requires two waves of glycoprotein synthesis, the first occurring immediately after training, and the second some 6 hr thereafter. The glycoprotein synthesis inhibitor 2-deoxygalactose results in amnesia if injected at either time, whereas the neural cell adhesion molecule (N-CAM) is specifically involved only in the second wave. The coincidence of the time course of memory disruption resulting from injection of L1 antibodies with that occurring with 2-deoxygalactose supports the hypothesis that establishment of an enduring memory for the experience of passive avoidance training requires two waves of glycoprotein synthesis, each wave being biochemically and functionally discrete. The differential effects of the two L1 fragments suggests that separate mechanisms of synaptic stabilization are involved at the two time points.

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Section: Introductionmentioning

confidence: 99%

A role for a chicken homolog of the neural cell adhesion molecule L1 in consolidation of memory for a passive avoidance task in the chick.

Scholey¹,

Mileusnic²,

Schachner³

et al. 1995

Learn. Mem.

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“…L1 also binds heterophili-cally to axonin-1, TAG-I, F3/Fll, and phosphacan (34,71). L1 regulates axon targeting, axon fasciculation, cell migration, and synaptic plasticity (3,36,38,39,51,71). Interactions of L1 with the fibroblast growth factor receptor (13,77) and pp60 ~src (25) appear to play an important role in its morphogenetic actions.…”

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confidence: 99%

“…Calcium-independent binding of L1 molecules in adjacent membranes (homophilic binding) promotes cell-cell adhesion and activates a tyrosine kinase signaling cascade involved in neurite outgrowth (36,77,79,81). L1 also binds heterophili-cally to axonin-1, TAG-I, F3/Fll, and phosphacan (34,71). L1 regulates axon targeting, axon fasciculation, cell migration, and synaptic plasticity (3,36,38,39,51,71).…”

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confidence: 99%

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Alcohol inhibits cell-cell adhesion mediated by human L1 [published erratum appears in J Cell Biol 1996 Jun;133(5):1139-40]

Ramanathan

Wilkemeyer

Mittal

et al. 1996

The Journal of Cell Biology

167

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Abstract. Mental retardation, hydrocephalus, and agenesis of the corpus callosum are observed both in fetal alcohol syndrome (FAS) and in children with mutations in the gene for the cell adhesion molecule L1. We studied the effects of ethanol on cell-cell adhesion in mouse fibroblasts transfected with human L1. Ll-transfected fibroblasts exhibited increased cell-cell adhesion compared with wild-type or vector-transfected controls. Ethanol potently and completely inhibited Ll-mediated adhesion both in transfected L cells and NIH/3T3 cells. Half-maximal inhibition was observed at 7 mM ethanol, a concentration achieved in blood and brain after ingesting one alcoholic beverage. In contrast, ethanol did not inhibit the adhesion of fibroblasts transfected with vector alone or with N-CAM-140. Ll-mediated cell-cell adhesion was inhibited with increasing potency by n-propanol and n-butanol, but was not inhibited at all by n-alcohols of 5 to 8 carbons, acetaldehyde, or acetate, suggesting that ethanol interacts directly with a small hydrophobic pocket within L1. Phenylalanine, teratogenic anticonvulsants, and high concentrations of glucose did not inhibit Ll-mediated cell-cell adhesion. Ethanol also inhibited potently the heterotypic adhesion of rat cerebellar granule cells to a monolayer of Ll-transfected NIH/3T3 cells, but had no effect on their adhesion to N-CAM-140 or vector-transfected NIH/3T3 cells. Because L1 plays a role in both neural development and learning, ethanol inhibition of Ll-mediated cell-cell interactions could contribute to FAS and ethanol-associated memory disorders. FETAL alcohol syndrome (FAS) 1 is one of the most common recognizable syndromes associated with mental retardation in the Western world (1). The full syndrome, characterized by growth retardation, neurological abnormalities, and facial malformations, occurs in N5% of the offspring of alcoholic women (1, 72). Neuropathological examination and neuroimaging of children with FAS have disclosed a spectrum of neurodevelopmental abnormalities, including hydrocephalus, agenesis of the corpus callosum, neuronal-glial heterotopias, cerebellar dysplasia, and microcephaly (8,27,62). Some of these lesions arise from disordered migration of neural cells, which has also been demonstrated experimentally in animal models of FAS (45,46 X-linked syndrome associated with mutations in the gene encoding L1, an immunoglobulin cell adhesion molecule (IgCAM) (4,20,28,31,66,74,83). Three overlapping syndromes, X-linked hydrocephalus, MASA syndrome (mental retardation, aphasia, shuffling gait, and adducted thumbs), and X-linked complicated spastic paraplegia, were each mapped to the same region (Xq28) of the X chromosome (32,76,82). A large number of different missense mutations, short deletions, and defects of alternative splicing within the L1 gene have been identified in individuals with these X-linked disorders (83); similar mutations have never been encountered in large numbers of control subjects. A single point mutation in L1 can cause either X-linked hydro...

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“…Axon-associated cell-adhesion molecules (AxCAMs), concentrated primarily on axons and growth cones, are known to play a prominent role in pathfinding decisions influenced by the local environment. AxCAMs are divided in three major groups; cadherins (Takeichi et al, 1991 ;Ranscht et al, 1994), integrins (Reichardt and Tomaselli, 1991) and neural surface proteins of the immunoglobulin superfamily (Sonderegger and Rathjen, 1992;Brummendorf and Rathjen, 1993). One subgroup of the Ig superfamily consists of Fll(contactin)/F3, TAG-l/axonin-1 and PANGBIG-I (Briimmendorf et al, 1989;Ranscht, 1988;Gennarini et al, 1989;Furley et al, 1990;Zuellig et al, 1992;Connelly et al, 1994;Yoshihara et al, 1994).…”

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The Neuronal Cell‐Adhesion Molecule Axonin‐1 is Specifically Released by an Endogenous Glycosylphosphatidylinositol‐Specific Phospholipase

Lierheimer

Kunz

Vogt

et al. 1997

European Journal of Biochemistry

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Axonin-I , a member of the immunoglobulidfibronectin type-I11 family of cell-adhesion molecules, occurs both as a glycosylphosphatidylinositol-(glycosylPtdIns)-anchored membrane-bound and a soluble form. In vivo observations show that the major part of axonin-1 is found in the soluble fraction and that soluble axonin-I perturbs neurite fasciculation and pathfinding in the developing chicken embryo. This has prompted further investigations into the mechanism of the axonin-I release. We demonstrate here that axonin-1 released from dorsal root ganglion neurons contains ethanolamine and inositol, components of the glycosylPtdIns anchor. Secreted axonin-1 does not exhibit the cross-reacting determinant epitope, an indication that the cleavage of the anchor is not mediated by a phosphatidylinositol-specific phospholipase C. Treatment of dorsal root ganglion neurons with 1,lO-phenanthroline, an inhibitor of glycosylPtdIns-specific phospholipase D, reduces the release of axonin-I by 56 %. Moreover, glycosylPtdIns-specific phospholipase D activity was detected in dorsal root ganglion neurons and brain. These results suggest that axonin-1 is released from the membrane by an endogenously expressed glycosylPtdIns-specific phospholipase D in viva With domain-swaping experiments between axonin-1 and its non-released relative F1 1, deletion mutants and monoclonal antibodies, we demonstrate that the fourth fibronectin type-111-like domain of axonin-I is required for the generation of the soluble form of axonin-1.

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Regulation of axonal growth in the vertebrate nervous system by interactions between glycoproteins belonging to two subgroups of the immunoglobulin superfamily.

Abstract: We acknowledge the critical reading of the manuscript of Drs. Klaus Hermann, Thomas Jentsch, Colin Henehan, and Brian Boycott. We would also like to thank Dagmar Boshold and Ursula Sogo for secretarial assistance, and Dr. Stephan Klauser for helping us with figures.

Cited by 152 publications

References 97 publications

A role for a chicken homolog of the neural cell adhesion molecule L1 in consolidation of memory for a passive avoidance task in the chick.

A role for a chicken homolog of the neural cell adhesion molecule L1 in consolidation of memory for a passive avoidance task in the chick.

Alcohol inhibits cell-cell adhesion mediated by human L1 [published erratum appears in J Cell Biol 1996 Jun;133(5):1139-40]

The Neuronal Cell‐Adhesion Molecule Axonin‐1 is Specifically Released by an Endogenous Glycosylphosphatidylinositol‐Specific Phospholipase

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