Lipid Raft-dependent Endocytosis of Close Homolog of Adhesion Molecule L1 (CHL1) Promotes Neuritogenesis

Tian, Nan; Leshchyns’ka, Iryna; Welch, Jeffrey; Diakowski, Witold; Yang, Hongyuan; Schachner, Melitta; Sytnyk, Vladimir

doi:10.1074/jbc.m112.394973

Cited by 28 publications

(35 citation statements)

References 51 publications

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“…During development the endocytosis of receptors and their ligands is an important signaling mechanism, which promotes neuronal differentiation, migration, neuritogenesis and outgrowth, and axon guidance (Itofusa, 2011; Kawauchi, 2012; Tian et al, 2012; Zhang et al, 2000). Pharmacological inhibition of endocytosis increases surface localization of FGFR1 and increases FGF2-dependent axon branching, suggesting that basal endocytosis of the receptor reduces FGF dependent axon branching (Hausott et al, 2011).…”

Section: Endocytosismentioning

confidence: 99%

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Winkle

Gupton

2016

International Review of Cell and Molecular Biology

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During development, neurons progress through rapid yet stereotypical shape changes to achieve proper neuronal connectivity. This morphological progression requires carefully orchestrated plasma membrane expansion, insertion of membrane components including receptors for extracellular cues into the plasma membrane and removal and trafficking of membrane materials and proteins to specific locations. This review outlines the cellular machinery of membrane trafficking that play an integral role in neuronal cell shape change and function from initial neurite formation to pathway navigation and synaptogenesis.

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Section: Endocytosismentioning

confidence: 99%

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Winkle

Gupton

2016

International Review of Cell and Molecular Biology

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“…21, 22, 23 We recently utilized LCLs from unrelated healthy individuals for conducting a genome-wide transcriptomic microarray based search for SSRI sensitivity biomarkers and reported several genes as tentative SSRI response biomarkers. 24, 25 Among these, CHL1 , coding for a cell adhesion protein implicated in neurogenesis and synaptogenesis, 26, 27, 28 seems a promising biomarker, as it is essential for correct neuronal wiring from the thalamus to the prefrontal cortex, 29 a neuronal pathway crucial for mood control. Moreover, CHL1 was reported as a potential SSRI sensitivity biomarker in a large study in major depression patients.…”

Section: Introductionmentioning

confidence: 99%

Genome-wide expression profiling of human lymphoblastoid cell lines implicates integrin beta-3 in the mode of action of antidepressants

et al. 2013

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Selective serotonin reuptake inhibitors (SSRIs) are the first-line treatment for major depression. However, the link between inhibition of serotonin reuptake and remission from depression remains controversial: in spite of the rapid onset of serotonin reuptake inhibition, remission from depression takes several weeks, presumably reflecting synaptogenesis/neurogenesis and neuronal rewiring. We compared genome-wide expression profiles of human lymphoblastoid cell lines from unrelated individuals following treatment with 1 μM paroxetine for 21 days with untreated control cells and examined which genes and microRNAs (miRNAs) showed the most profound and consistent expression changes. ITGB3, coding for integrin beta-3, showed the most consistent altered expression (1.92-fold increase, P=7.5 × 10−8) following chronic paroxetine exposure. Using genome-wide miRNA arrays, we observed a corresponding decrease in the expression of two miRNAs, miR-221 and miR-222, both predicted to target ITGB3. ITGB3 is crucial for the activity of the serotonin transporter (SERT), the drug target of SSRIs. Moreover, it is presumably required for the neuronal guidance activity of CHL1, whose expression was formerly identified as a tentative SSRI response biomarker. Further genes whose expression was significantly modulated by chronic paroxetine are also implicated in neurogenesis. Surprisingly, the expression of SERT or serotonin receptors was not modified. Our findings implicate ITGB3 in the mode of action of SSRI antidepressants and provide a novel link between CHL1 and the SERT. Our observations suggest that SSRIs may relieve depression primarily by promoting neuronal synaptogenesis/neurogenesis rather than by modulating serotonin neurotransmission per se.

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“…Hence, we compared endocytosis rates of hNCAM180 and hNCAMΔCT by analyzing the internalization of NCAM antibodies in live CHO cells, an assay used by us previously to analyze endocytosis of CHL1, another cell adhesion molecule of the immunoglobulin superfamily (Tian et al, 2012). Transfected CHO cells were incubated with antibodies recognizing the extracellular domain of hNCAM.…”

Section: Ncam Colocalizes With Kinesin-1 In Trans-golgi Organellesmentioning

confidence: 99%

“…The PLA was performed as described previously (Li et al, 2013;Tian et al, 2012). Cultured neurons were fixed in 4% formaldehyde in PBS, washed with PBS, permeabilized with 0.25% Triton X-100 in PBS for 5 min, blocked with 1% BSA in PBS for 20 min, and incubated with antibodies against the intracellular domain of NCAM and KLC1 or KLC2 applied in 0.1% BSA in PBS overnight at 4°C.…”

Section: Proximity Ligation Assaymentioning

confidence: 99%

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Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

Wobst

Schmitz

Schachner

et al. 2015

Journal of Cell Science

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The neural cell adhesion molecule (NCAM, also known as NCAM1) is important during neural development, because it contributes to neurite outgrowth in response to its ligands at the cell surface. In the adult brain, NCAM is involved in regulating synaptic plasticity. The molecular mechanisms underlying delivery of NCAM to the neuronal cell surface remain poorly understood. We used a protein macroarray and identified the kinesin light chain 1 (KLC1), a component of the kinesin-1 motor protein, as a binding partner of the intracellular domains of the two transmembrane isoforms of NCAM, NCAM140 and NCAM180. KLC1 binds to amino acids CGKAGPGA within the intracellular domain of NCAM and colocalizes with kinesin-1 in the Golgi compartment. Delivery of NCAM180 to the cell surface is increased in CHO cells and neurons co-transfected with kinesin-1. We further demonstrate that the p21-activated kinase 1 (PAK1) competes with KLC1 for binding to the intracellular domain of NCAM and contributes to the regulation of the membrane insertion of NCAM. Our results indicate that NCAM is delivered to the cell surface through a kinesin-1-mediated transport mechanism in a PAK1-dependent manner.

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Lipid Raft-dependent Endocytosis of Close Homolog of Adhesion Molecule L1 (CHL1) Promotes Neuritogenesis

Cited by 28 publications

References 51 publications

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Membrane Trafficking in Neuronal Development: Ins and Outs of Neural Connectivity

Genome-wide expression profiling of human lymphoblastoid cell lines implicates integrin beta-3 in the mode of action of antidepressants

Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

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