Shuichi Hayashi
   Department     Kawasaki Medical School, Department of Anatomy,
   Position   Associate Professor
Article types 原著
Language English
Peer review Peer reviewed
Title Protocadherin-17 mediates collective axon extension by recruiting actin regulator complexes to interaxonal contacts.
Journal Formal name:Developmental Cell
Domestic / ForeginForegin
Volume, Issue, Page 30(6),673-687頁
Author and coauthor Hayashi, S., Inoue, Y., Kiyonari, H., Abe, T., Misaki, K., Moriguchi, H., Tanaka, Y. and Takeichi, M.
Publication date 2014
Summary In the process of neuronal wiring, axons derived from the same functional group typically extend together, resulting in fascicle formation. How these axons communicate with one another remains largely unknown. Here, we show that protocadherin-17 (Pcdh17) supports this group extension by recruiting actin polymerization regulators to interaxonal contact sites. Pcdh17 is expressed by a subset of amygdala neurons, and it accumulates at axon-axon boundaries because of homophilic binding. Pcdh17 knockout in mice suppressed the extension of these axons. Ectopically expressed Pcdh17 altered the pattern of axon extension. In in-vitro cultures, wild-type growth cones normally migrate along other axons, whereas Pcdh17 null growth cones do not. Pcdh17 recruits the WAVE complex, Lamellipodin, and Ena/VASP to cell-cell contacts, converting these sites into motile structures. We propose that, through these mechanisms, Pcdh17 maintains the migration of growth cones that are in contact with other axons, thereby supporting their collective extension.