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Neural Adhesion Molecules—from Development to Adult Synaptic Plasticity
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Neural Adhesion Molecules—from Development to Adult Synaptic Plasticity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 5117

Special Issue Editor

Prof. Dr. Melitta Schachner

E-Mail Website
Guest Editor
W. M. Keck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08554, USA
Interests: nervous system; cell adhesion molecules; development; synaptic function and plasticity; recovery after trauma; spinal cord injury; traumatic brain injury; neurodegenerative diseases; microglia; mitochondria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since the discovery of the first neural cell adhesion molecule in Gerald Edelman's group about 50 years ago, the neural cell adhesion molecule NCAM was introduced as a 'glue' that prevents the brain from falling apart. Soon thereafter, L1CAM (L1 in short) was described as contributing to neuronal cell migration along radial glial fibers in the developing murine cerebellum. Sequence analysis revealed that they belong to the immunoglobulin superfamily. Furthermore, their covalently attached carbohydrates were shown to be functionally important. These carbohydrates formed the basis for the discovery of new adhesion molecules (CAMs) that do not belong to the immunoglobulin superfamily: integrins, selectins, and cadherins, to name only a few. Transmembrane CAMs signal to the cell interior, thereby shaping a cell's response to ligand triggering. Depending on the ligand, responses can lead to agonistic or antagonistic effects on cell migration, neurite outgrowth, neuronal survival, synapse formation, synaptic plasticity, and overall regeneration after trauma. As well as neurons, glia also express CAMs. Of note, many such molecules are present in the extracellular space, where they react with each other or bind to their receptors at the cell surface. CAMs also determine the functions of tumors. Last, but not least, mutations in CAMs lead to neural and non-neural diseases, since non-neural cells also express CAMs that were initially characterized in the nervous system. The aim of this Special Issue is to illustrate the manifold features of CAMs.

Prof. Dr. Melitta Schachner
Guest Editor

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Keywords

  • neural cell adhesion
  • radial glial fiber
  • CAMs

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Published Papers (3 papers)

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Research

19 pages, 4431 KiB  
Article
The CHD Protein Kismet Restricts the Synaptic Localization of Cell Adhesion Molecules at the Drosophila Neuromuscular Junction
by Ireland R. Smith, Emily L. Hendricks, Nina K. Latcheva, Daniel R. Marenda and Faith L. W. Liebl
Int. J. Mol. Sci. 2024, 25(5), 3074; https://doi.org/10.3390/ijms25053074 - 6 Mar 2024
Cited by 1 | Viewed by 1694
Abstract
The appropriate expression and localization of cell surface cell adhesion molecules must be tightly regulated for optimal synaptic growth and function. How neuronal plasma membrane proteins, including cell adhesion molecules, cycle between early endosomes and the plasma membrane is poorly understood. Here we [...] Read more.
The appropriate expression and localization of cell surface cell adhesion molecules must be tightly regulated for optimal synaptic growth and function. How neuronal plasma membrane proteins, including cell adhesion molecules, cycle between early endosomes and the plasma membrane is poorly understood. Here we show that the Drosophila homolog of the chromatin remodeling enzymes CHD7 and CHD8, Kismet, represses the synaptic levels of several cell adhesion molecules. Neuroligins 1 and 3 and the integrins αPS2 and βPS are increased at kismet mutant synapses but Kismet only directly regulates transcription of neuroligin 2. Kismet may therefore regulate synaptic CAMs indirectly by activating transcription of gene products that promote intracellular vesicle trafficking including endophilin B (endoB) and/or rab11. Knock down of EndoB in all tissues or neurons increases synaptic FasII while knock down of EndoB in kis mutants does not produce an additive increase in FasII. In contrast, neuronal expression of Rab11, which is deficient in kis mutants, leads to a further increase in synaptic FasII in kis mutants. These data support the hypothesis that Kis influences the synaptic localization of FasII by promoting intracellular vesicle trafficking through the early endosome. Full article
(This article belongs to the Special Issue Neural Adhesion Molecules—from Development to Adult Synaptic Plasticity)
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13 pages, 3357 KiB  
Article
Single Nucleotide Polymorphism in Cell Adhesion Molecule L1 Affects Learning and Memory in a Mouse Model of Traumatic Brain Injury
by Haoyu Jiang, Anna O. Giarratana, Thomas Theis, Vini Nagaraj, Xiaofeng Zhou, Smita Thakker-Varia, Melitta Schachner and Janet Alder
Int. J. Mol. Sci. 2024, 25(5), 3043; https://doi.org/10.3390/ijms25053043 - 6 Mar 2024
Cited by 1 | Viewed by 1270
Abstract
The L1 cell adhesion molecule (L1) has demonstrated a range of beneficial effects in animal models of spinal cord injury, neurodegenerative disease, and ischemia; however, the role of L1 in TBI has not been fully examined. Mutations in the L1 gene affecting the [...] Read more.
The L1 cell adhesion molecule (L1) has demonstrated a range of beneficial effects in animal models of spinal cord injury, neurodegenerative disease, and ischemia; however, the role of L1 in TBI has not been fully examined. Mutations in the L1 gene affecting the extracellular domain of this type 1 transmembrane glycoprotein have been identified in patients with L1 syndrome. These patients suffer from hydrocephalus, MASA (mental retardation, adducted thumbs, shuffling gait, aphasia) symptoms, and corpus callosum agenesis. Clinicians have observed that recovery post-traumatic brain injury (TBI) varies among the population. This variability may be explained by the genetic differences present in the general population. In this study, we utilized a novel mouse model of L1 syndrome with a mutation at aspartic acid position 201 in the extracellular domain of L1 (L1-201). We assessed the impact of this specific single nucleotide polymorphism (SNP) localized to the X-chromosome L1 gene on recovery outcomes following TBI by comparing the L1-201 mouse mutants with their wild-type littermates. We demonstrate that male L1-201 mice exhibit significantly worse learning and memory outcomes in the Morris water maze after lateral fluid percussion (LFP) injury compared to male wild-type mice and a trend to worse motor function on the rotarod. However, no significant changes were observed in markers for inflammatory responses or apoptosis after TBI. Full article
(This article belongs to the Special Issue Neural Adhesion Molecules—from Development to Adult Synaptic Plasticity)
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18 pages, 2585 KiB  
Article
Interaction of L1CAM with LC3 Is Required for L1-Dependent Neurite Outgrowth and Neuronal Survival
by Gabriele Loers, Ralf Kleene, Viviana Granato, Ute Bork and Melitta Schachner
Int. J. Mol. Sci. 2023, 24(15), 12531; https://doi.org/10.3390/ijms241512531 - 7 Aug 2023
Cited by 3 | Viewed by 1417
Abstract
The neural cell adhesion molecule L1 (also called L1CAM or CD171) functions not only in cell migration, but also in cell survival, differentiation, myelination, neurite outgrowth, and signaling during nervous system development and in adults. The proteolytic cleavage of L1 in its extracellular [...] Read more.
The neural cell adhesion molecule L1 (also called L1CAM or CD171) functions not only in cell migration, but also in cell survival, differentiation, myelination, neurite outgrowth, and signaling during nervous system development and in adults. The proteolytic cleavage of L1 in its extracellular domain generates soluble fragments which are shed into the extracellular space and transmembrane fragments that are internalized into the cell and transported to various organelles to regulate cellular functions. To identify novel intracellular interaction partners of L1, we searched for protein–protein interaction motifs and found two potential microtubule-associated protein 1 light-chain 3 (LC3)-interacting region (LIR) motifs within L1, one in its extracellular domain and one in its intracellular domain. By ELISA, immunoprecipitation, and proximity ligation assay using L1 mutant mice lacking the 70 kDa L1 fragment (L1-70), we showed that L1-70 interacts with LC3 via the extracellular LIR motif in the fourth fibronectin type III domain, but not by the motif in the intracellular domain. The disruption of the L1-LC3 interaction reduces L1-mediated neurite outgrowth and neuronal survival. Full article
(This article belongs to the Special Issue Neural Adhesion Molecules—from Development to Adult Synaptic Plasticity)
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