Dynamic regulation of cell adhesion molecules during axon outgrowth

Long, Kristin E.; Lemmon, Vance

doi:10.1002/1097-4695(200008)44:2<230::aid-neu12>3.0.co;2-w

Cited by 28 publications

(21 citation statements)

References 123 publications

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“…The process of cell migration requires dynamic regulation of cell adhesion through coupling of adhesion receptors with the cytoskeleton (74,75). The motif FIGQY in the cytoplasmic domain motif of all L1 family members except CHL1 is part of the binding site for ankyrin, a multivalent adapter of the spectrin/actin cortical skeleton (18).…”

Section: Discussionmentioning

confidence: 99%

Close Homolog of L1 Is an Enhancer of Integrin-mediated Cell Migration

Buhusi

Midkiff

Gates

et al. 2003

Journal of Biological Chemistry

106

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Close homolog of L1 (CHL1) is a member of the L1 family of cell adhesion molecules expressed by subpopulations of neurons and glia in the central and peripheral nervous system. It promotes neurite outgrowth and neuronal survival in vitro. This study describes a novel function for CHL1 in potentiating integrin-dependent cell migration toward extracellular matrix proteins. Expression of CHL1 in HEK293 cells stimulated their haptotactic migration toward collagen I, fibronectin, laminin, and vitronectin substrates in Transwell assays. CHL1-potentiated cell migration to collagen I was dependent on ␣ 1 ␤ 1 and ␣ 2 ␤ 1 integrins, as shown with function blocking antibodies. Potentiated migration relied on the early integrin signaling intermediates c-Src, phosphatidylinositol 3-kinase, and mitogen-activated protein kinase. Enhancement of migration was disrupted by mutation of a potential integrin interaction motif Asp-Gly-Glu-Ala (DGEA) in the sixth immunoglobulin domain of CHL1, suggesting that CHL1 functionally interacts with ␤ 1 integrins through this domain. CHL1 was shown to associate with ␤ 1 integrins on the cell surface by antibody-induced co-capping. Through a cytoplasmic domain sequence containing a conserved tyrosine residue (Phe-Ile-Gly-Ala-Tyr), CHL1 recruited the actin cytoskeletal adapter protein ankyrin to the plasma membrane, and this sequence was necessary for promoting integrin-dependent migration to extracellular matrix proteins. These results support a role for CHL1 in integrin-dependent cell migration that may be physiologically important in regulating cell migration in nerve regeneration and cortical development.

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Section: Discussionmentioning

confidence: 99%

Close Homolog of L1 Is an Enhancer of Integrin-mediated Cell Migration

Buhusi

Midkiff

Gates

et al. 2003

Journal of Biological Chemistry

106

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“…The location, levels, and residence time of adhesion and guidance receptors crucially influence their functional activity (Long and Lemmon 2000) and hence axon guidance and growth. This is similar to cell migration in which it is thought that targeted recruitment of adhesion molecules, like integrins, to the cell's leading edge promotes directional movement of the cell (Bretscher and Aguado-Velasco 1998).…”

Section: Local Control Of Guidance Receptor Distribution At Growth Conesmentioning

confidence: 99%

Trafficking Guidance Receptors

Winckler

Mellman²

2010

Cold Spring Harbor Perspectives in Biology

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Wiring of the brain relies initially on the correct outgrowth of axons to reach the appropriate target area for innervation. A large number of guidance receptors present in the plasma membrane of axonal growth cones and elsewhere on the neuron read and execute directional cues present in the extracellular environment of the navigating growth cone. The exact timing, levels, and localization of expression of the guidance receptors in the plasma membrane therefore determine the outcome of guidance decisions. Many guidance receptors are localized in exquisitely precise spatial and temporal patterns. The cellular mechanisms ensuring these localization patterns include spatially accurate sorting after synthesis in the secretory pathway, retrieval of inappropriately expressed receptors by endocytosis followed by degradation or recycling, and restriction of diffusion. This article will discuss the machinery and regulation underlying the restricted distribution of membrane receptors, focusing on the currently best-studied example, the L1 cell adhesion molecule. In addition to the longrange mechanisms ensuring appropriate localization, the same mechanisms can act locally to adjust levels and localization of receptors. These local mechanisms are regulated by ligand binding and subsequent activation of local signaling cascades. It is likely that the localization of all guidance receptors is regulated by a combination of sorting, retrieval, recycling and retention, similar to the ones we discuss here for L1.

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“…Rap1 itself plays a role in the activation of the NGF-dependent ERK pathway, leading to axonal elongation in PC-12 cells (26). The cell adhesion molecule Ninjurin has also been reported to be induced by peripheral nerve injury, and promotes axonal and neurite outgrowth in sciatic nerve and DRG neurons following injury (20,35).…”

Section: Coronin 1b and Rab13 Protein Expression Is Induced After Scmentioning

confidence: 99%

In Vivo and in Vitro Characterization of Novel Neuronal Plasticity Factors Identified following Spinal Cord Injury

Giovanni

Biase

Yakovlev

et al. 2005

Journal of Biological Chemistry

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Following spinal cord injury, there are numerous changes in gene expression that appear to contribute to either neurodegeneration or reparative processes. We utilized high density oligonucleotide microarrays to examine temporal gene profile changes after spinal cord injury in rats with the goal of identifying novel factors involved in neural plasticity. By comparing mRNA changes that were coordinately regulated over time with genes previously implicated in nerve regeneration or plasticity, we found a gene cluster whose members are involved in cell adhesion processes, synaptic plasticity, and/or cytoskeleton remodeling. This group, which included the small GTPase Rab13 and actin-binding protein Coronin 1b, showed significantly increased mRNA expression from 7-28 days after trauma. Overexpression in vitro using PC-12, neuroblastoma, and DRG neurons demonstrated that these genes enhance neurite outgrowth. Moreover, RNAi gene silencing for Coronin 1b or Rab13 in NGF-treated PC-12 cells markedly reduced neurite outgrowth. Coronin 1b and Rab13 proteins were expressed in cultured DRG neurons at the cortical cytoskeleton, and at growth cones along with the pro-plasticity/regeneration protein GAP-43. Finally, Coronin 1b and Rab13 were induced in the injured spinal cord, where they were also co-expressed with GAP-43 in neurons and axons. Modulation of these proteins may provide novel targets for facilitating restorative processes after spinal cord injury.Traumatic injury to the spinal cord induces delayed biochemical responses that affect both cell loss and subsequent repair. Modulation of reparative processes includes factors involved in either facilitating or inhibiting neurite outgrowth, which are often regulated at the gene and protein levels after injury. Collectively, these factors likely determine in part the degree of anatomical and functional recovery after injury.Regeneration-associated proteins (RAGs) appear to play a role in plasticity and regeneration following SCI. 1 These include transcription factors (c-Jun), cytoskeletal components (T␣1), microtubule-associated proteins, growth-associated proteins (GAP-43, CAP-23), cell adhesion molecules (N-CAM, L1, TAG1), neurotrophic factors, cytokines, and extracellular matrix components (SNAP25, munc13, and cpg15/neuritin) (1-10). In some cases, these factors share common molecular pathways. GAP-43 and CAP-23 bind downstream to the cofactor PI(4,5)P(2), at plasmalemmal rafts, contributing to the regulation of actin and modulating neurite outgrowth in neuronallike cell lines (11,12). In other instances, a common downstream effector, such as neurotrophin-dependent intracellular cAMP, may serve to facilitate axonal regeneration by overcoming inhibition from factors such as myelin-associated glycoprotein (MAG) (13)(14)(15).Microarray technology provides a powerful tool for identifying molecular pathways involved in either endogenous neurotoxicity or regeneration/plasticity after SCI (16 -19). It allows concurrent analysis of thousands of genes and the identification of c...

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Dynamic regulation of cell adhesion molecules during axon outgrowth

Cited by 28 publications

References 123 publications

Close Homolog of L1 Is an Enhancer of Integrin-mediated Cell Migration

Close Homolog of L1 Is an Enhancer of Integrin-mediated Cell Migration

Trafficking Guidance Receptors

In Vivo and in Vitro Characterization of Novel Neuronal Plasticity Factors Identified following Spinal Cord Injury

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