ハヤシ シュウイチ
  林 周一
   所属   川崎医科大学  医学部 基礎医学 解剖学
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Protocadherin-17 mediates collective axon extension by recruiting actin regulator complexes to interaxonal contacts.
掲載誌名 正式名:Developmental Cell
掲載区分国外
巻・号・頁 30(6),673-687頁
著者・共著者 Hayashi, S., Inoue, Y., Kiyonari, H., Abe, T., Misaki, K., Moriguchi, H., Tanaka, Y. and Takeichi, M.
発行年月 2014
概要 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.