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Neural recognition molecules CHL1 and NB‐3 regulate apical dendrite orientation in the neocortex via PTPα
Author(s) -
Ye Haihong,
Tan Yen Ling Jessie,
Ponniah Sathivel,
Takeda Yasuo,
Wang ShiQiang,
Schachner Melitta,
Watanabe Kazutada,
Pallen Catherine J,
Xiao ZhiCheng
Publication year - 2008
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601939
Subject(s) - neocortex , biology , apical dendrite , dendrite (mathematics) , cortex (anatomy) , neuroscience , microbiology and biotechnology , pyramidal cell , neurogenesis , anatomy , cerebral cortex , hippocampal formation , geometry , mathematics
Apical dendrites of pyramidal neurons in the neocortex have a stereotypic orientation that is important for neuronal function. Neural recognition molecule Close Homolog of L1 (CHL1) has been shown to regulate oriented growth of apical dendrites in the mouse caudal cortex. Here we show that CHL1 directly associates with NB‐3, a member of the F3/contactin family of neural recognition molecules, and enhances its cell surface expression. Similar to CHL1, NB‐3 exhibits high‐caudal to low‐rostral expression in the deep layer neurons of the neocortex. NB‐3‐deficient mice show abnormal apical dendrite projections of deep layer pyramidal neurons in the visual cortex. Both CHL1 and NB‐3 interact with protein tyrosine phosphatase α (PTPα) and regulate its activity. Moreover, deep layer pyramidal neurons of PTPα‐deficient mice develop misoriented, even inverted, apical dendrites. We propose a signaling complex in which PTPα mediates CHL1 and NB‐3‐regulated apical dendrite projection in the developing caudal cortex.