Neural cell adhesion molecules modulate tyrosine phosphorylation of tubulin in nerve growth cone membranes

Atashi, Julie R.; Klinz, Stephan G.; Ingraham, Christine A.; Matten, Wayne T.; Schachner, Melitta; Maness, Patricia F.

doi:10.1016/0896-6273(92)90197-l

Cited by 194 publications

(104 citation statements)

References 66 publications

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“…Cross-linking of some proteins to either ligand or antibody can result in their enhanced partitioning into rafts and participation in early signaltransduction events (Simons and Toomre, 2000). Previous studies have validated the use of antibodies to mimic ligand binding (Atashi et al, 1992;Simons and Toomre, 2000;Filatov et al, 2003). For example, we have shown that whereas ∼40% of MOG in myelin is associated with detergent-insoluble complexes that are characteristic of rafts, MOG in OLs in culture is nearly entirely excluded from rafts (Marta et al, 2003).…”

Section: Introductionmentioning

confidence: 77%

Myelin associated glycoprotein cross-linking triggers its partitioning into lipid rafts, specific signaling events and cytoskeletal rearrangements in oligodendrocytes

Marta

Taylor²,

Cheng³

et al. 2004

Neuron Glia Biol.

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Myelin-associated glycoprotein (MAG) has been implicated in inhibition of nerve regeneration in the CNS. This results from interactions between MAG and the Nogo receptor and gangliosides on the apposing axon, which generates intracellular inhibitory signals in the neuron. However, because myelin-axon signaling is bidirectional, we undertook an analysis of potential MAG-activated signaling in oligodendrocytes (OLs). In this study, we show that antibody cross-linking of MAG on the surface of OLs (to mimic axonal binding) leads to the redistribution of MAG into detergent (TX-100)-insoluble complexes, hyperphosphorylation of Fyn, dephosphorylation of serine and threonine residues in specific proteins, including lactate dehydrogenase and the β subunit of the trimeric G-protein-complex, and cleavage of α-fodrin followed by a transient depolymerization of actin. We propose that these changes are part of a signaling cascade in OLs associated with MAG function as a mediator of axon-glial communication which might have implications for the mutual regulation of the formation and stability of axons and myelin.

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Section: Introductionmentioning

confidence: 77%

Myelin associated glycoprotein cross-linking triggers its partitioning into lipid rafts, specific signaling events and cytoskeletal rearrangements in oligodendrocytes

Marta

Taylor²,

Cheng³

et al. 2004

Neuron Glia Biol.

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“…The functional significance of MOG-tubulin association was indicated due to anti-MOG antibody induced β-tubulin dephosphorylation and repartition of MOG and β-tubulin into lipid rafts following MOG signaling in cultured oligodendrocytes (Marta et al 2003). Dephosphorylation of β-tubulin has been shown to interfere with the microtubule stability (Atashi et al 1992) and may be involved in the organization of myelin. Here we show that both MOG and β-tubulin are differentially distributed in WT and GMF-KO myelin fractions.…”

Section: Discussionmentioning

confidence: 99%

Diminished degradation of myelin basic protein by anti-sulfatide antibody and interferon-γ in myelin from glia maturation factor-deficient mice

Menon

Haas

et al. 2007

Neuroscience Research

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In this study we show the effect of anti-sulfatide (RmAb) antibodies and inflammatory cytokines, TNF-α and IFN-γ in inducing myelin basic protein (MBP) degradation in myelin isolated from control wild type (WT) and glia maturation factor (GMF)-deficient (GMF-KO) mice. GMF was not detected in isolated myelin from WT and GMF-KO mice although it is present in brains of WT mice. Our results show that calcium dependent neutral protease activity caused significantly elevated degradation of 18.5 and/or 17.5 kDa isoforms of MBP in WT-myelin treated with RmAb or IFN-γ. In contrast, MBP degradation in isolated myelin from GMF-KO mice remained unaffected following treatment with RmAb, IFN-γ, or GM-CSF. Neither the 14 kDa isoform of MBP or proteolipid protein (PLP) showed an elevated degradation compared to controls. A virtual absence of GM-CSF, TNF-α and IFN-γ in GMF-KO brain compared to WT was also evident when the animals were challenged with MOG 35-55. Additionally, the myelin from GMF-KO mice showed difference in distribution of myelin oligodendrocyte glycoprotein (MOG) and β-tubulin in a sucrose density gradient myelinaxolemmal fractions compared to WT. Taken together, our data suggests a role for GMF in the biochemical organization of myelin and thereby its effect on MBP degradation induced by RmAb and IFN-γ.

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“…The effects on different second messenger systems are also functionally discrete; in all cell types examined L1 and N-CAM affected inositol phosphate breakdown, levels of cellular calcium and changes in intracellular pH, whereas levels of cAMP were raised in cerebellar neurons only, an effect not observed in response to N-CAM (von Bohlen und Halbach et al 1992). Both L1 and N-CAM inhibit the phosphorylation of tyrosine residues in nerve growth cones (Atashi et al 1992), a phenomenon that may be related to the stabilization of the neuronal cytoskeleton. It may be relevant that there is an increase in tyrosinated e~-tubulin immunoreactivity in both left IMHV and right LPO by 6 hr post-training--an increase not apparent in these regions at 1 hr post-training (Scholey et al 1992)--and that may accompany the second wave of glycoprotein synthesis and could feasibly be mediated by both N-CAM and L1.…”

Section: Discussionmentioning

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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Neural cell adhesion molecules modulate tyrosine phosphorylation of tubulin in nerve growth cone membranes

Cited by 194 publications

References 66 publications

Myelin associated glycoprotein cross-linking triggers its partitioning into lipid rafts, specific signaling events and cytoskeletal rearrangements in oligodendrocytes

Myelin associated glycoprotein cross-linking triggers its partitioning into lipid rafts, specific signaling events and cytoskeletal rearrangements in oligodendrocytes

Diminished degradation of myelin basic protein by anti-sulfatide antibody and interferon-γ in myelin from glia maturation factor-deficient mice

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.

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