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Molecular and Cellular Biology, November 2002, p. 7967-7981, Vol. 22, No. 22
0270-7306/02/$04.00+0 DOI: 10.1128/MCB.22.22.7967-7981.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Misguided Axonal Projections, Neural Cell Adhesion Molecule 180 mRNA Upregulation, and Altered Behavior in Mice Deficient for the Close Homolog of L1
M. Montag-Sallaz,1,2 M. Schachner,2,3 and D. Montag1,2*
Neurogenetics Research Group, Leibniz Institute for Neurobiology, D-39118 Magdeburg,1
Zentrum für Molekulare Neurobiologie, Universitäts-Krankenhaus, Eppendorf, D-20246 Hamburg, Germany,3
Department of Neurobiology, Swiss Federal Institute of Technology, Hoenggerberg, CH 8093 Zurich, Switzerland2
Received 4 April 2002/
Returned for modification 4 June 2002/
Accepted 15 August 2002
Cell recognition molecules are involved in nervous system development and participate in synaptic plasticity in the adult brain. The close homolog of L1 (CHL1), a recently identified member of the L1 family of cell adhesion molecules, is expressed by neurons and glia in the central nervous system and by Schwann cells in the peripheral nervous system in a pattern overlapping, but distinct from, the other members of the L1 family. In humans, CHL1 (also referred to as CALL) is a candidate gene for 3p- syndrome-associated mental impairment. In the present study, we generated and analyzed CHL1-deficient mice. At the morphological level, these mice showed alterations of hippocampal mossy fiber organization and of olfactory axon projections. Expression of the mRNA of the synapse-specific neural cell adhesion molecule 180 isoform was upregulated in adult CHL1-deficient mice, but the mRNA levels of several other recognition molecules were not changed. The behavior of CHL1-deficient mice in the open field, the elevated plus maze, and the Morris water maze indicated that the mutant animals reacted differently to their environment. Our data show that the permanent absence of CHL1 results in misguided axonal projections and aberrant axonal connectivity and alters the exploratory behavior in novel environments, suggesting deficits in information processing in CHL1-deficient mice.
* Corresponding author. Mailing address: Neurogenetics Research Group, Leibniz Institute for Neurobiology, D-39118 Magdeburg, Germany. Phone: 49-391-6263215. Fax: 49-391-6263252. E-mail:
montag{at}ifn-magdeburg.de.
Molecular and Cellular Biology, November 2002, p. 7967-7981, Vol. 22, No. 22
0022-538X/02/$04.00+0 DOI: 10.1128/MCB.22.22.7967-7981.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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