Shuichi Hayashi    Department   Kawasaki Medical School  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 / Foregin	Foregin
Volume, Issue, Page	30(6),pp.673-687
Author and coauthor	Hayashi, S., Inoue, Y., Kiyonari, H., Abe, T., Misaki, K., Moriguchi, H., Tanaka, Y. and Takeichi, M.
Authorship	Lead author
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.