Characterization of functional domains of the tenascin-R (restrictin) polypeptide: cell attachment site, binding with F11, and enhancement of F11-mediated neurite outgrowth by tenascin-R.

Nörenberg, Ursel; Hubert, Michael; Brümmendorf, Thomas; Tárnok, Attila; Rathjen, Fritz G.

doi:10.1083/jcb.130.2.473

Cited by 57 publications

(51 citation statements)

References 59 publications

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“…However, microglial cells that ramify at L1 can then resume their radial migration to reach L2 (interface between sublayers within the IPL) and L3 (IPL-INL interface) by traversing the tenascinrich territory of the IPL. This would be explained by the presence in the tenascin molecule of domains with opposite functions, adhesive and antiadhesive Norenberg et al, 1995;Faissner, 1997;Ghert et al, 2001), and by the ability of this molecule to bind to different receptors (Schnapp et al, 1995;Mackie, 1997;Zacharias et al, 1999;Pesheva and Probstmeier, 2000). Therefore, tenascin is able to exert both inhibitory and stimulatory effects on cell migration (Faissner, 1997).…”

Section: Possible Involvement Of Tenascin In Stopping and Ramificatiomentioning

confidence: 99%

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

Sánchez‐López

Cuadros

Calvente

et al. 2004

Glia

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Microglial cells spread within the nervous system by tangential and radial migration. The cellular mechanism of tangential migration of microglia has been described in the quail retina but the mechanism of their radial migration has not been studied. In this work, we clarify some aspects of this mechanism by analyzing morphological features of microglial cells at different steps of their radial migration in the quail retina. Microglial cells migrate in the vitreal half of the retina by successive jumps from the vitreal border to progressively more scleral levels located at the vitreal border, intermediate regions, and scleral border of the inner plexiform layer (IPL). The cellular mechanism used for each jump consists of the emission of a leading thin radial process that ramifies at a more scleral level before retraction of the rear of the cell. Hence, radial migration and ramification of microglial cells are simultaneous events. Once at the scleral border of the IPL, microglial cells migrate through the inner nuclear layer to the outer plexiform layer by another mechanism: they retract cell processes, become round, and squeeze through neuronal bodies. Microglial cells use radial processes of s-lamininexpressing Mü ller cells as substratum for radial migration. Levels where microglial cells stop and ramify at each jump are always interfaces between retinal strata with strong tenascin immunostaining and strata showing weak or no tenascin immunoreactivity. When microglial cell radial migration ends, tenascin immunostaining is no longer present in the retina. These findings suggest that tenascin plays a role in the stopping and ramification of radially migrating microglial cells.

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Section: Possible Involvement Of Tenascin In Stopping and Ramificatiomentioning

confidence: 99%

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

Sánchez‐López

Cuadros

Calvente

et al. 2004

Glia

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“…The parallel defects in Cntn1-KO mice with this latter phenotype raise the possibility that axonal Contactin, in addition to its role at paranodes, participates in stabilizing nodal complexes through NF186 or ECM interactions. Indeed, several studies documented Contactin interactions with various cytoskeleton-associated membrane proteins and ECM components, including neurofascins, NgCAM, NrCAM, RPTP-β/phosphacan, tenascin-R, and tenascin-C (32)(33)(34)(51)(52)(53).…”

Section: Contactin In Domain Organization Of Myelinated Central Nervesmentioning

confidence: 99%

Contactin-1 regulates myelination and nodal/paranodal domain organization in the central nervous system

Çolakoğlu

Bergstrom-Tyrberg

Berglund

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Myelin, a multilayered membrane sheath formed by oligodendrocytes around axons in the CNS, enables rapid nerve impulse conduction and sustains neuronal health. The signals exchanged between axons and oligodendrocytes in myelin remain to be fully elucidated. Here we provide genetic evidence for multiple and critical functions of Contactin-1 in central myelin. We document dynamic Contactin-1 expression on oligodendrocytes in vivo, and progressive accumulation at nodes of Ranvier and paranodes during postnatal mouse development. Nodal and paranodal expression stabilized in mature myelin, but overall membranous expression diminished. Contactin-1-deficiency disrupted paranodal junction formation as evidenced by loss of Caspr, mislocalized potassium K v 1.2 channels, and abnormal myelin terminal loops. Reduced numbers and impaired maturation of sodium channel clusters accompanied this phenotype. Histological, electron microscopic, and biochemical analyses uncovered significant hypomyelination in Contactin-1-deficient central nerves, with up to 60% myelin loss. Oligodendrocytes were present in normal numbers, albeit a minor population of neuronal/glial antigen 2-positive (NG2 + ) progenitors lagged in maturation by postnatal day 18, when the mouse null mutation was lethal. Major contributing factors to hypomyelination were defects in the generation and organization of myelin membranes, as judged by electron microscopy and quantitative analysis of oligodendrocyte processes labeled by GFP transgenically expressed from the proteolipid protein promoter. These data reveal that Contactin-1 regulates both myelin formation and organization of nodal and paranodal domains in the CNS. These multiple roles distinguish central Contactin-1 functions from its specific role at paranodes in the periphery, and emphasize mechanistic differences in central and peripheral myelination.

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“…For example, TN-C and TN-R contain both adhesive and counteradhesive sites for cell attachment. TN-C is able to stimulate neurite outgrowth (30), and TN-R has been shown to enhance neurite growth mediated by other substrates and to modulate the cellular receptor usage that is responsible for mediating the outgrowth effect (31,32).…”

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confidence: 99%

CALEB Binds via Its Acidic Stretch to the Fibrinogen-like Domain of Tenascin-C or Tenascin-R and Its Expression Is Dynamically Regulated after Optic Nerve Lesion

Schumacher

Jung

Nörenberg

et al. 2001

Journal of Biological Chemistry

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Recently, we described a novel chick neural transmembrane glycoprotein, which interacts with the extracellular matrix proteins tenascin-C and tenascin-R. This protein, termed CALEB, contains an epidermal growth factor-like domain and appears to be a novel member of the epidermal growth factor family of growth and differentiation factors. Here we analyze the interaction between CALEB and tenascin-C as well as tenascin-R in more detail, and we demonstrate that the central acidic peptide segment of CALEB is necessary to mediate this binding. The fibrinogen-like globe within tenascin-C or -R enables both proteins to bind to CALEB. We show that two isoforms of CALEB in chick and rodents exist that differed in their cytoplasmic segments. To begin to understand the in vivo function of CALEB and since in vitro antibody perturbation experiments indicated that CALEB might be important for neurite formation, we analyzed the expression pattern of the rat homolog of CALEB during development of retinal ganglion cells, after optic nerve lesion and during graft-assisted retinal ganglion cell axon regeneration by in situ hybridization. These investigations demonstrate that CALEB mRNA is dynamically regulated after optic nerve lesion and that this mRNA is expressed in most developing and in onethird of the few regenerating (GAP-43 expressing) retinal ganglion cells.

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Characterization of functional domains of the tenascin-R (restrictin) polypeptide: cell attachment site, binding with F11, and enhancement of F11-mediated neurite outgrowth by tenascin-R.

Cited by 57 publications

References 59 publications

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

Contactin-1 regulates myelination and nodal/paranodal domain organization in the central nervous system

CALEB Binds via Its Acidic Stretch to the Fibrinogen-like Domain of Tenascin-C or Tenascin-R and Its Expression Is Dynamically Regulated after Optic Nerve Lesion

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