PT  - JOURNAL ARTICLE
AU  - Hua-Li Yu
AU  - Yun Peng
AU  - Yang Zhao
AU  - Yong-Sheng Lan
AU  - Bo Wang
AU  - Lu Zhao
AU  - Dong Sun
AU  - Jin-Xiu Pan
AU  - Zhao-Qi Dong
AU  - Lin Mei
AU  - Yu-Qiang Ding
AU  - Xiao-Juan Zhu
AU  - Wen-Cheng Xiong
TI  - Myosin X interaction with KIF13B, a crucial pathway for Netrin-1-induced axonal development
AID  - 10.1101/2020.01.06.896100
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.01.06.896100
4099  - http://biorxiv.org/content/early/2020/01/06/2020.01.06.896100.short
4100  - http://biorxiv.org/content/early/2020/01/06/2020.01.06.896100.full
AB  - Myosin X (Myo X) transports cargos to the tip of filopodia for cell adhesion, migration, and neuronal axon guidance. Deleted in Colorectal Cancer (DCC) is one of Myo X cargos essential for Netrin-1-regulated axon pathfinding. Myo X’s function in axon development in vivo and the underlying mechanisms remain poorly understood. Here, we provide evidence for Myo X’s function in Netrin-1-DCC regulated axon development in mouse neocortex. Knocking-out (KO) or knocking-down (KD) Myo X in embryonic cortical neurons impairs axon initiation and contralateral branching/targeting. Similar axon deficits are detected in Netrin-1-KO or DCC-KD cortical neurons. Myo X interacts with KIF13B (a kinesin family motor protein), which is induced by Netrin-1. Netrin-1 promotes anterograde transportation of Myo X into axons in KIF13B dependent manner. KIF13B-KD cortical neurons exhibit similar axon deficits. These results suggest Myo X-KIF13B as a critical pathway for Netrin-1 promoted axon initiation and branching/targeting.