Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 2, Pages 395-403Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4097-04.2005
Keywords
L1CAM; neurite outgrowth; ERM proteins; axon branching; juxtamembrane; ankyrin; adhesion
Categories
Funding
- NEI NIH HHS [R01 EY005285-23, R01 EY005285, EY-11373, EY-05285, P30 EY011373] Funding Source: Medline
- NICHD NIH HHS [R01 HD039884-06, HD39884, R01 HD039884] Funding Source: Medline
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We investigated how the neural cell adhesion molecule L1 mediates neurite outgrowth through L1-L1 homophilic interactions. Wild-type L1 and L1 with mutations in the cytoplasmic domain (CD) were introduced into L1 knock-out neurons, and transfected neurons were grown on an L1 substrate. Neurite length and branching were compared between wild-type L1 and L1CD mutations. Surprisingly, the L1CD is not required for L1-mediated neurite outgrowth but plays a critical role in neurite branching, through both the juxtamembrane region and the RSLE region. We demonstrate that both regions serve as ezrin-moesin-radixin-binding sites. A truncation mutant that deletes 110 of 114 amino acids of the L1CD still supports neurite outgrowth on an L1 substrate, suggesting that a coreceptor binds to L1 in cis and mediates neurite outgrowth and that L1-ankyrin interactions are not essential for neurite initiation or outgrowth. These data are consistent with a model in which L1 can influence L1-mediated neurite outgrowth and branching through both the L1CD and a coreceptor.
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