Shootin1-cortactin interaction mediates signal-force transduction for axon outgrowth

• Kubo, Yusuke

• Baba, Kentarou

• Toriyama, Michinori

• Minegishi, Takunori

• Sugiura, Tadao

• Kozawa, Satoshi

• Ikeda, Kazushi

• Inagaki, Naoyuki

抄録

Motile cells transduce environmental chemical signals into mechanical forces to achieve properly controlled migration. This signal-force transduction is thought to require regulated mechanical coupling between actin filaments (F-actins), which undergo retrograde flow at the cellular leading edge, and cell adhesions via linker "clutch" molecules. However, the molecular machinery mediating this regulatory coupling remains unclear. Here we show that the F-actin binding molecule cortactin directly interacts with a clutch molecule, shootin1, in axonal growth cones, thereby mediating the linkage between F-actin retrograde flow and cell adhesions through L1-CAM. Shootin1-cortactin interaction was enhanced by shootin1 phosphorylation by Pak1, which is activated by the axonal chemoattractant netrin-1. We provide evidence that shootin1-cortactin interaction participates in netrin-1-induced F-actin adhesion coupling and in the promotion of traction forces for axon outgrowth. Under cell signaling, this regulatory F-actin adhesion coupling in growth cones cooperates with actin polymerization for efficient cellular motility.

収録刊行物

• The Journal of Cell Biology

  The Journal of Cell Biology 210 (4), 663-676, 2015-08-17

  The Rockefeller University Press

キーワード

• Cell Biology

詳細情報

• CRID: 1050577309352874880
• NII論文ID: 120005716857
• NII書誌ID: AA00694812
• ISSN: 15408140
• ISSN: 00219525
• DOI: 10.1083/jcb.201505011
• HANDLE: 10061/10086
• Web Site: https://naist.repo.nii.ac.jp/records/9121
• Web Site: https://rupress.org/jcb/article-pdf/210/4/663/1593290/jcb_201505011.pdf
• 本文言語コード: en
• 資料種別: journal article
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