Journal Article 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

2015-08-17 , The Rockefeller University Press
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.

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