Brain development in mice lacking L1-L1 homophilic adhesion

Kyoko Itoh, Ling Cheng, Yoshimasa Kamei, Shinji Fushiki, Hiroyuki Kamiguchi, Paul Gutwein, Alexander Stoeck, Bernd Arnold, Peter Altevogt, Vance Lemmon

Research output: Contribution to journalArticlepeer-review

70 Scopus citations


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-α5β1 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-α5β1 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.

Original languageEnglish (US)
Pages (from-to)145-154
Number of pages10
JournalJournal of Cell Biology
Issue number1
StatePublished - Apr 12 2004


  • Adhesion
  • Corticospinal tract
  • Hydrocephalus
  • Integrin
  • L1 cam

ASJC Scopus subject areas

  • Cell Biology


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