Migration of F9 parietal endoderm cells is regulated by the ERK pathway

✍ Scribed by Tao Hong; Laura B. Grabel

• Book ID: 102302692
• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 486 KB
• Volume: 97
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.20728

✦ Synopsis

Abstract

Cell migration is regulated by the action of many signaling pathways that are activated in specific regions of migrating cells. Extracellular regulated kinase 1/2 (ERK) signaling can modulate the migration of cells by controlling the turnover of focal adhesions and the dynamics of actin polymerization. Focal adhesion turnover is necessary for cell migration, and the formation of strong actin stress fibers and mature focal adhesions puts the brakes on cell migration. We used F9 wild‐type and vinculin null (vin^−/−^) parietal endoderm (PE) outgrowth to study the role of the ERK signaling pathway in cell migration. Upon plating of F9 embryoid bodies (EBs) onto laminin‐coated dishes, PE cells migrate away from the EBs, providing an in vitro model for studying directed migration of this embryonic cell type. Our results suggest that the ERK pathway regulates PE cell migration by affecting the formation of focal adhesions and lamellipodia through the action of myosin light chain kinase (MLCK). J. Cell. Biochem. 97: 1339–1349, 2006. © 2005 Wiley‐Liss, Inc.