Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 5978K) PPT slides of all figures Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Itoh, K. Articles by Lemmon, V. Search for Related Content PubMed PubMed Citation Articles by Itoh, K. Articles by Lemmon, V. Related Collections Related Article Social Bookmarking                            What's this?

Brain development in mice lacking L1–L1 homophilic adhesion

¹ Department of Neuroscience, Case Western Reserve University, Cleveland, OH 44106
² Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine, Kyoto 602-0841, Japan
³ Developmental Brain Science Group, RIKEN Brain Science Institute, Saitama 351-0198, Japan
⁴ D010, German Cancer Research Center, D-69120 Heidelberg, Germany
⁵ D050 Tumor Immunology Program, German Cancer Research Center, D-69120 Heidelberg, Germany
⁶ The Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, FL 33136

Address correspondence to Vance Lemmon, The Miami Project to Cure Paralysis, University of Miami School of Medicine, Lois Pope LIFE Center, Room 4-16, 1095 NW 14th Terrace, Miami, FL 33136. Tel.: (305) 243-6793. Fax: (305) 243-3160. email: vlemmon{at}miami.edu

A new mouse line has been produced in which the sixth Ig domain of the L1 cell adhesion molecule has been deleted. Despite the rather large deletion, L1 expression is preserved at normal levels. In vitro experiments showed that L1–L1 homophilic binding was lost, along with L1-5ß1 integrin binding. However, L1–neurocan and L1–neuropilin binding were preserved and sema3a responses were intact. Surprisingly, many of the axon guidance defects present in the L1 knockout mice, such as abnormal corticospinal tract and corpus callosum, were not observed. Nonetheless, when backcrossed on the C57BL/6 strain, a severe hydrocephalus was observed and after several generations, became an embryonic lethal. These results imply that L1 binding to L1, TAG-1, or F3, and L1-5ß1 integrin binding are not essential for normal development of a variety of axon pathways, and suggest that L1–L1 homophilic binding is important in the production of X-linked hydrocephalus.

Key Words: adhesion; hydrocephalus; L1cam; corticospinal tract; integrin

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

Related Article

Brain construction goes straight

William A. Wells
J. Cell Biol. 2004 165: 15. [Full Text] [PDF]

This article has been cited by other articles:

• Nagaraj, K., Kristiansen, L. V., Skrzynski, A., Castiella, C., Garcia-Alonso, L., Hortsch, M. (2009). Pathogenic human L1-CAM mutations reduce the adhesion-dependent activation of EGFR. Hum Mol Genet 18: 3822-3831 [Abstract] [Full Text]  
• Guseva, D., Angelov, D. N., Irintchev, A., Schachner, M. (2009). Ablation of adhesion molecule L1 in mice favours Schwann cell proliferation and functional recovery after peripheral nerve injury. Brain 132: 2180-2195 [Abstract] [Full Text]  
• Amano, K., Fujii, M., Arata, S., Tojima, T., Ogawa, M., Morita, N., Shimohata, A., Furuichi, T., Itohara, S., Kamiguchi, H., Korenberg, J. R., Arata, A., Yamakawa, K. (2009). DSCAM Deficiency Causes Loss of Pre-Inspiratory Neuron Synchroneity and Perinatal Death. J. Neurosci. 29: 2984-2996 [Abstract] [Full Text]  
• Gouveia, R. M., Gomes, C. M., Sousa, M., Alves, P. M., Costa, J. (2008). Kinetic Analysis of L1 Homophilic Interaction: ROLE OF THE FIRST FOUR IMMUNOGLOBULIN DOMAINS AND IMPLICATIONS ON BINDING MECHANISM. J. Biol. Chem. 283: 28038-28047 [Abstract] [Full Text]  
• Rantakari, P., Strauss, L., Kiviranta, R., Lagerbohm, H., Paviala, J., Holopainen, I., Vainio, S., Pakarinen, P., Poutanen, M. (2008). Placenta Defects and Embryonic Lethality Resulting from Disruption of Mouse Hydroxysteroid (17-{beta}) Dehydrogenase 2 Gene. Mol. Endocrinol. 22: 665-675 [Abstract] [Full Text]  
• Wolman, M. A., Regnery, A. M., Becker, T., Becker, C. G., Halloran, M. C. (2007). Semaphorin3D Regulates Axon Axon Interactions by Modulating Levels of L1 Cell Adhesion Molecule. J. Neurosci. 27: 9653-9663 [Abstract] [Full Text]  
• Dequidt, C., Danglot, L., Alberts, P., Galli, T., Choquet, D., Thoumine, O. (2007). Fast Turnover of L1 Adhesions in Neuronal Growth Cones Involving Both Surface Diffusion and Exo/Endocytosis of L1 Molecules. Mol. Biol. Cell 18: 3131-3143 [Abstract] [Full Text]  
• Sweger, E. J., Casper, K. B., Scearce-Levie, K., Conklin, B. R., McCarthy, K. D. (2007). Development of Hydrocephalus in Mice Expressing the Gi-Coupled GPCR Ro1 RASSL Receptor in Astrocytes. J. Neurosci. 27: 2309-2317 [Abstract] [Full Text]  
• Weinhold, B., Seidenfaden, R., Rockle, I., Muhlenhoff, M., Schertzinger, F., Conzelmann, S., Marth, J. D., Gerardy-Schahn, R., Hildebrandt, H. (2005). Genetic Ablation of Polysialic Acid Causes Severe Neurodevelopmental Defects Rescued by Deletion of the Neural Cell Adhesion Molecule. J. Biol. Chem. 280: 42971-42977 [Abstract] [Full Text]  
• Maretzky, T., Schulte, M., Ludwig, A., Rose-John, S., Blobel, C., Hartmann, D., Altevogt, P., Saftig, P., Reiss, K. (2005). L1 Is Sequentially Processed by Two Differently Activated Metalloproteases and Presenilin/{gamma}-Secretase and Regulates Neural Cell Adhesion, Cell Migration, and Neurite Outgrowth. Mol. Cell. Biol. 25: 9040-9053 [Abstract] [Full Text]  
• Cheng, L., Itoh, K., Lemmon, V. (2005). L1-Mediated Branching Is Regulated by Two Ezrin-Radixin-Moesin (ERM)-Binding Sites, the RSLE Region and a Novel Juxtamembrane ERM-Binding Region. J. Neurosci. 25: 395-403 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents