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International Journal Of Bilogical Sciences

.: Home > International Journal Of Bilogical Sciences > 2013 > Volume 9 Number 8 > Hyejin Oh1, Hwan Kim1, Baehyun Shin2, Kun Ho Lee3, Myeong Gu Yeo4 ✉, Woo Keun Song1✉

Interaction of Crk with Myosin-1c Participates in Fibronectin-Induced Cell Spreading

Hyejin Oh1, Hwan Kim1, Baehyun Shin2, Kun Ho Lee3, Myeong Gu Yeo4 ✉, Woo Keun Song1✉
1. Bio Imaging and Cell Dynamics Research Center, 2. Bio Remodeling and Gene Therapy Lab., School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea, 3. Department of Marine Biology, Chosun University, Gwangju, 501-759, Korea 4. Department of Alternative Medicine, Nambu University, Gwangju 506-706, Korea
Abstract :

We previously reported a novel interaction between v-Crk and myosin-1c, and demonstrated that this interaction is essential for cell migration, even in the absence of p130CAS. We here demonstrate a role for Crk-myosin-1c interaction in cell adhesion and spreading. Crk-knockout (Crk‑/‑) mouse embryo fibroblasts (MEFs) exhibited significantly decreased cell spreading and reduced Rac1 activity. A stroboscopic analysis of cell dynamics during cell spreading revealed that the cell-spreading deficiency in Crk‑/‑ MEFs was due to the short protrusion/retraction distances and long persistence times of membrane extensions. The low activity of Rac1 in Crk‑/‑ MEFs, which led to delayed cell spreading in these cells, is consistent with the observed defects in membrane dynamics. Reintroduction of v-Crk into Crk‑/‑ MEFs rescued these defects, restoring cell-spreading activity and membrane dynamics to Crk+/+ MEF levels, and normalizing Rac1 activity. Knockdown of myosin-1c by introduction of small interfering RNA resulted in a delay in cell spreading and reduced Rac1 activity to low levels, suggesting that myosin-1c also plays an essential role in cell adhesion and spreading. In addition, deletion of the v-Crk SH3 domain, which interacts with the myosin-1c tail, led to defects in cell spreading. Overexpression of the GFP-myosin-1c tail domain effectively inhibited the v-Crk-myosin-1c interaction and led to a slight decrease in cell spreading and cell surface area. Collectively, these findings suggest that the v-Crk-myosin-1c interaction, which modulates membrane dynamics by regulating Rac1 activity, is crucial for cell adhesion and spreading.

Keywords :
v-Crk, myosin-1c, cell adhesion, cell spreading

Date Deposited : 11 Apr 2015 10:35

Last Modified : 11 Apr 2015 10:35

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Volume 9, Number 8, - 2013 , ISSN 1449-2288

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