期刊
TRAFFIC
卷 18, 期 5, 页码 287-303出版社
WILEY
DOI: 10.1111/tra.12473
关键词
AP-2 adaptor complex; cell adhesion; endocytosis; N-cadherin; -catenin; 2 subunit
类别
资金
- Ministry of Science and Technology [NSC99-2321-B-001-018-MY3]
- National Health Research Institutes [NHRI99-EX99-9919NC]
- Integrated Thematic Project of Academia Sinica [AS100-TP-B09]
- Institute of Molecular Biology
Circuit formation in the brain requires neurite outgrowth throughout development to establish synaptic contacts with target cells. Active endocytosis of several adhesion molecules facilitates the dynamic exchange of these molecules at the surface and promotes neurite outgrowth in developing neurons. The endocytosis of N-cadherin, a calcium-dependent adhesion molecule, has been implicated in the regulation of neurite outgrowth, but the mechanism remains unclear. Here, we identified that a fraction of N-cadherin internalizes through clathrin-mediated endocytosis (CME). Two tyrosine-based motifs in the cytoplasmic domain of N-cadherin recognized by the 2 subunit of the AP-2 adaptor complex are responsible for CME of N-cadherin. Moreover, -catenin, a core component of the N-cadherin adhesion complex, inhibits N-cadherin endocytosis by masking the 2 tyrosine-based motifs. Removal of -catenin facilitates 2 binding to N-cadherin, thereby increasing clathrin-mediated N-cadherin endocytosis and neurite outgrowth without affecting the steady-state level of surface N-cadherin. These results identify and characterize the mechanism controlling N-cadherin endocytosis through -catenin-regulated 2 binding to modulate neurite outgrowth.
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