ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
No Nogo66- and NgR-mediated inhibition of regenerating axons in the zebrafish optic nerve.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Axonal defasciculation is restricted to specific branching points during regeneration of the lateral line nerve in zebrafish.Development (Cambridge, England) · 2026Article
- Elevated phagocytic capacity directs innate spinal cord repair.Cell reports · 2026Article
- Shared diagnostic biomarkers and diagnostic models of age-related macular degeneration and systemic lupus erythematosus.International ophthalmology · 2026Article
- Axonal defasciculation is restricted to specific branching points during regeneration of the lateral line nerve in zebrafish.bioRxiv : the preprint server for biology · 2025Article
- Article
- Zebrafish Spinal Cord Repair Is Accompanied by Transient Tissue Stiffening.Biophysical journal · 2020Article
- Soluble Nogo receptor 1 fusion protein protects neural progenitor cells in rats with ischemic stroke.Neural regeneration research · 2019Article
- Conditional Overexpression of rtn4al in Muscle of Adult Zebrafish Displays Defects Similar to Human Amyotrophic Lateral Sclerosis.Marine biotechnology (New York, N.Y.) · 2019Article
- Optic nerve regeneration: A long view.Restorative neurology and neuroscience · 2019Review
- Axonal regeneration in zebrafish spinal cord.Regeneration (Oxford, England) · 2018Review
- RTN1-C mediates cerebral ischemia/reperfusion injury via ER stress and mitochondria-associated apoptosis pathways.Cell death & disease · 2017Article
- Inhibition of Reticulon-1A-Mediated Endoplasmic Reticulum Stress in Early AKI Attenuates Renal Fibrosis Development.Journal of the American Society of Nephrology : JASN · 2017Article
- Knockdown of RTN1A attenuates ER stress and kidney injury in albumin overload-induced nephropathy.American journal of physiology. Renal physiology · 2016Article
- RTN1 mediates progression of kidney disease by inducing ER stress.Nature communications · 2015Article
- Upregulation of the zebrafish Nogo-A homologue, Rtn4b, in retinal ganglion cells is functionally involved in axon regeneration.Neural development · 2015Article
- Essential roles of zebrafish rtn4/Nogo paralogues in embryonic development.Neural development · 2014Article
- Reggies/flotillins interact with Rab11a and SNX4 at the tubulovesicular recycling compartment and function in transferrin receptor and E-cadherin trafficking.Molecular biology of the cell · 2013Article
- Axonal regeneration after spinal cord injury in zebrafish and mammals: differences, similarities, translation.Neuroscience bulletin · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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