RRC ID 31990
著者 Hayashi S, Inoue Y, Kiyonari H, Abe T, Misaki K, Moriguchi H, Tanaka Y, Takeichi M.
タイトル Protocadherin-17 mediates collective axon extension by recruiting actin regulator complexes to interaxonal contacts.
ジャーナル Dev Cell
Abstract 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.
巻・号 30(6)
ページ 673-87
公開日 2014-9-29
DOI 10.1016/j.devcel.2014.07.015
PII S1534-5807(14)00457-2
PMID 25199687
MeSH Actins / metabolism* Amygdala / cytology Amygdala / growth & development Amygdala / metabolism Animals Axons / metabolism* Axons / physiology Cadherins / genetics Cadherins / metabolism* Cell Movement DNA-Binding Proteins / metabolism Growth Cones / metabolism* Growth Cones / physiology Mice Protocadherins Wiskott-Aldrich Syndrome Protein Family / metabolism
IF 10.092
引用数 45
WOS 分野 DEVELOPMENTAL BIOLOGY CELL BIOLOGY
リソース情報
遺伝子材料 pCAH-Pcdh17-EGFP (RDB13049) pCAP-Lamellipodin-His (RDB13050).