Defects in Cell Adhesion and the Visceral Endoderm following Ablation of Nonmuscle Myosin Heavy Chain II-A in Mice

Conti MA, Even-Ram S, Liu C, Yamada KM and Adelstein RS
Source: J Biol Chem
Publication Date: (2004)
Issue: 279(40): 41263-41266
Research Area:
Cancer Research/Cell Biology
Cells used in publication:
Embryonic stem cell (ES), mouse
Species: mouse
Tissue Origin: embryo
Nucleofectorâ„¢ I/II/2b
Here we show that mice ablated for NMHC II-A fail to develop a normal patterned embryo with a polarized visceral endoderm by E6.5 and die by E7.5. Moreover, A(-)/A(-) embryoid bodies grown in suspension culture constantly shed cells. These defects in cell adhesion and tissue organization are explained by loss of E-cadherin and beta-catenin localization to cell adhesion sites in both cell culture and in the intact embryos. The defects can be reproduced by introducing siRNA directed against NMHC II-A into wild-type embryonic stem cells. Our results suggest an essential role for a single, specific nonmuscle myosin isoform in maintaining cell-cell adhesions in the early mammalian embryo.