Skip Navigation



MBE Advance Access published online on August 29, 2003
Molecular Biology and Evolution, doi:10.1093/molbev/msg241
Molecular Biology and Evolution © Society for Molecular Biology and Evolution 2003; all rights reserved
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
21/1/76    most recent
msg241v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Klinger, M.
Right arrow Articles by Diekmann, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Klinger, M.
Right arrow Articles by Diekmann, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Accepted August 7, 2003
© 2003 Society for Molecular Biology and Evolution

Original Articles

Identification of Nogo-66 Receptor (NgR) and Homologous Genes in Fish

Michael Klinger 1, John S. Taylor 2, Thomas Oertle 3, Martin E. Schwab 3, Claudia A. O. Stuermer 1, and Heike Diekmann 1*

1 Department of Biology, University of Konstanz, 78457 Konstanz, Germany
2 Department of Biology, University of Victoria, Victoria, BC, V8W 3N5, Canada
3 Department of Biology, ETH Zurich and Brain Research Institute, University of Zurich, 8057 Zurich, Switzerland

* To whom correspondence should be addressed. E-mail: heike.diekmann{at}uni-konstanz.de.


  Abstract

The Nogo-66 receptor NgR has been implicated in the mediation of inhibitory effects of central nervous system (CNS) myelin on axon growth in the adult mammalian CNS. NgR binds to several myelin-associated ligands (Nogo-66, myelin associated glycoprotein, oligodendrocyte-myelin glycoprotein) which - among other inhibitory proteins - impair axonal regeneration in the CNS of adult mammals. In contrast to mammals, severed axons readily regenerate in the fish CNS. Nevertheless, fish axons are repelled by mammalian oligodendrocytes in vitro. Therefore, the identification of fish NgR homologs is a crucial step towards understanding NgR functions in vertebrate systems competent of CNS regeneration. Here, we report the discovery of four zebrafish (Danio rerio) and five fugu (Takifugu rubripes) NgR homologs. Synteny between fish and human, comparable intron-exon structures and phylogenetic analyses provide convincing evidence that the true fish orthologs were identified. The topology of the phylogenetic trees shows that the extra fish genes were produced by duplication events that occurred in ray-finned fishes prior to the divergence of the zebrafish and pufferfish lineages. Expression of zebrafish NgR homologs was detected relatively early in development and prominently in the adult brain suggesting functions in axon growth, guidance or plasticity.

Key Words: NgR, Danio rerio, Fugu rubripes, Reticulon, gene duplication, conserved synteny


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol Biol EvolHome page
H. Diekmann, M. Klinger, T. Oertle, D. Heinz, H.-M. Pogoda, M. E. Schwab, and C. A. O. Stuermer
Analysis of the Reticulon Gene Family Demonstrates the Absence of the Neurite Growth Inhibitor Nogo-A in Fish
Mol. Biol. Evol., August 1, 2005; 22(8): 1635 - 1648.
[Abstract] [Full Text] [PDF]

Home page
 GlycobiologyHome page
F. Lehmann, H. Gathje, S. Kelm, and F. Dietz
Evolution of sialic acid-binding proteins: molecular cloning and expression of fish siglec-4
Glycobiology, November 1, 2004; 14(11): 959 - 968.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.