Features and Functions of Oligodendrocytes and Myelin Proteins of Lower Vertebrate Species

Jeserich, G.; Klempahn, Katrin; Pfeiffer, Melanie

doi:10.1007/s12031-008-9035-0

Cited by 25 publications

(23 citation statements)

References 81 publications

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“…Moreover, the fact that NgR signaling upon ZF-Nogo66 binding promotes growth predicts that additional ligands of NgR such as MAG, OMGP, and further myelin proteins negatively affecting axon growth in mammals (Yiu and He, 2006), probably have no or only weak inhibitory influence on axon growth in fish, or are simply absent (such as the NogoA-specific domain). In addition, fish possess their own myelin components such as the proteins 36k and IP-1 and IP-2 (Jeserich et al, 2008) that are absent from mammals. Furthermore, no glial scar-associated growth inhibition exists in goldfish (Hirsch et al, 1995) and glial cell-derived soluble factors actually support axon regeneration (Schwalb et al, 1996).…”

Section: Nogo-66 In the Path Of Regenerating Axonsmentioning

confidence: 99%

No Nogo66- and NgR-Mediated Inhibition of Regenerating Axons in the Zebrafish Optic Nerve

Abdesselem¹,

Shypitsyna²,

Solis³

et al. 2009

J. Neurosci.

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In contrast to mammals, lesioned axons in the zebrafish (ZF) optic nerve regenerate and restore vision. This correlates with the absence of the NogoA-specific N-terminal domains from the ZF nogo/rtn-4 (reticulon-4) gene that inhibits regeneration in mammals. However, mammalian nogo/rtn-4 carries a second inhibitory C-terminal domain, Nogo-66, being 70% identical with ZF-Nogo66. The present study examines, (1) whether ZF-Nogo66 is inhibitory and effecting similar signaling pathways upon Nogo66-binding to the Nogo66 receptor NgR and its coreceptors, and (2) whether Rat-Nogo66 on fish, and ZF-Nogo66 on mouse neurons, cause inhibition via NgR. Our results from "outgrowth, collapse and contact assays" suggest, surprisingly, that ZF-Nogo66 is growth-permissive for ZF and mouse neurons, quite in contrast to its Rat-Nogo66 homolog which inhibits growth. The opposite effects of ZF-and Rat-Nogo66 are, in both fish and mouse, transmitted by GPI (glycosylphosphatidylinositol)-anchored receptors, including NgR. The high degree of sequence homology in the predicted binding site is consistent with the ability of ZF-and mammalian-Nogo66 to bind to NgRs of both species. Yet, Rat-Nogo66 elicits phosphorylation of the downstream effector cofilin whereas ZF-Nogo66 has no influence on cofilin phosphorylation-probably because of significantly different Rat-versus ZF-Nogo66 sequences outside of the receptor-binding region effecting, by speculation, recruitment of a different set of coreceptors or microdomain association of NgR. Thus, not only was the NogoA-specific domain lost in fish, but Nogo66, the second inhibitory domain in mammals, and its signaling upon binding to NgR, was modified so that ZF-Nogo/RTN-4 does not impair axon regeneration.

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Section: Nogo-66 In the Path Of Regenerating Axonsmentioning

confidence: 99%

No Nogo66- and NgR-Mediated Inhibition of Regenerating Axons in the Zebrafish Optic Nerve

Abdesselem¹,

Shypitsyna²,

Solis³

et al. 2009

J. Neurosci.

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“…This suggests an evolutionary neuroprotective change in myelin chemistry between aquatic and terrestrial vertebrates, which is supported by the degenerative phenotype observed in transgenic mice that express P 0 instead of Plp in their CNS (Yin et al, 2006). Although there is sequence conservation between zebrafish and mammalian P 0 (Schweitzer et al, 2003), the zebrafish p 0 gene shows greater promoter region sequence conservation with the mammalian Plp gene rather than mammalian P 0 (Jeserich et al, 2008;Jeserich et al, 1997). In keeping with this, a zebrafish transgenic line, which expresses enhanced green fluorescent protein (EGFP) under the regulation of a mouse Plp promoter, exhibits strong EGFP expression in oligodendrocytes and their precursors, although it is not clear whether this promoter regulates zebrafish dm20 or p 0 genes (Yoshida and Macklin, 2005).…”

Section: Zebrafish and Mammalian Myelin: A Comparisonmentioning

confidence: 96%

“…The major biochemical difference between zebrafish and mammalian myelin is the presence of protein zero (P 0 ) as a major CNS myelin protein in zebrafish, rather than PLP in mammals (Table 1) (Jeserich et al, 2008;Waehneldt et al, 1986). This suggests an evolutionary neuroprotective change in myelin chemistry between aquatic and terrestrial vertebrates, which is supported by the degenerative phenotype observed in transgenic mice that express P 0 instead of Plp in their CNS (Yin et al, 2006).…”

Section: Zebrafish and Mammalian Myelin: A Comparisonmentioning

confidence: 99%

“…In keeping with this, a zebrafish transgenic line, which expresses enhanced green fluorescent protein (EGFP) under the regulation of a mouse Plp promoter, exhibits strong EGFP expression in oligodendrocytes and their precursors, although it is not clear whether this promoter regulates zebrafish dm20 or p 0 genes (Yoshida and Macklin, 2005). This suggests that there is not a clear biochemical distinction between oligodendrocytes and Schwann cells in the zebrafish (Jeserich et al, 2008).…”

Section: Zebrafish and Mammalian Myelin: A Comparisonmentioning

confidence: 99%

“…Nevertheless, the structural properties and cell lineage relationship of oligodendrocytes is highly comparable between zebrafish and mammals (Jeserich et al, 2008;Jeserich and Stratmann, 1992;Jeserich and Waehneldt, 1986;Sivron et al, 1990). Also, orthologous genes for all of the major mammalian myelinassociated genes have been found in zebrafish (dm20, mbp and p 0 ) (Brosamle and Halpern, 2002).…”

Section: Zebrafish and Mammalian Myelin: A Comparisonmentioning

confidence: 99%

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Zebrafish myelination: a transparent model for remyelination?

Buckley

Goldsmith²,

Franklin³

2008

Disease Models &Amp; Mechanisms

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There is currently an unmet need for a therapy that promotes the regenerative process of remyelination in central nervous system diseases, notably multiple sclerosis (MS). A high-throughput model is, therefore, required to screen potential therapeutic drugs and to refine genomic and proteomic data from MS lesions. Here, we review the value of the zebrafish (Danio rerio) larva as a model of the developmental process of myelination, describing the powerful applications of zebrafish for genetic manipulation and genetic screens, as well as some of the exciting imaging capabilities of this model. Finally, we discuss how a model of zebrafish myelination can be used as a high-throughput screening model to predict the effect of compounds on remyelination. We conclude that zebrafish provide a highly versatile myelination model. As more complex transgenic zebrafish lines are developed, it might soon be possible to visualise myelination, or even remyelination, in real time. However, experimental outputs must be designed carefully for such visual and temporal techniques.

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Peripheral axons of the adult zebrafish maxillary barbel extensively remyelinate during sensory appendage regeneration

Moore

Mark

Hogan

et al. 2012

J of Comparative Neurology

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Myelination is a cellular adaptation allowing rapid conduction along axons. We have investigated peripheral axons of the zebrafish maxillary barbel (ZMB), an optically clear sensory appendage. Each barbel carries taste buds, solitary chemosensory cells, and epithelial nerve endings, all of which regenerate after amputation (LeClair and Topczewski [2010] PLoS One 5:e8737). The ZMB contains axons from the facial nerve; however, myelination within the barbel itself has not been established. Transcripts of myelin basic protein (mbp) are expressed in normal and regenerating adult barbels, indicating activity in both maintenance and repair. Myelin was confirmed in situ by using toluidine blue, an anti-MBP antibody, and transmission electron microscopy (TEM). The adult ZMB contains ~180 small-diameter axons (<2 μm), approximately 60% of which are myelinated. Developmental myelination was observed via whole-mount immunohistochemistry 4-6 weeks postfertilization, showing myelin sheaths lagging behind growing axons. Early-regenerating axons (10 days postsurgery), having no or few myelin layers, were disorganized within a fibroblast-rich collagenous scar. Twenty-eight days postsurgery, barbel axons had grown out several millimeters and were organized with compact myelin sheaths. Fiber types and axon areas were similar between normal and regenerated tissue; within 4 weeks, regenerating axons restored ~85% of normal myelin thickness. Regenerating barbels express multiple promyelinating transcription factors (sox10, oct6 = pou3f1; krox20a/b = egr2a/b) typical of Schwann cells. These observations extend our understanding of the zebrafish peripheral nervous system within a little-studied sensory appendage. The accessible ZMB provides a novel context for studying axon regeneration, Schwann cell migration, and remyelination in a model vertebrate.

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Features and Functions of Oligodendrocytes and Myelin Proteins of Lower Vertebrate Species

Cited by 25 publications

References 81 publications

No Nogo66- and NgR-Mediated Inhibition of Regenerating Axons in the Zebrafish Optic Nerve

No Nogo66- and NgR-Mediated Inhibition of Regenerating Axons in the Zebrafish Optic Nerve

Zebrafish myelination: a transparent model for remyelination?

Peripheral axons of the adult zebrafish maxillary barbel extensively remyelinate during sensory appendage regeneration

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