PMID:15292239

Citation	Conti, MA, Even-Ram, S, Liu, C, Yamada, KM and Adelstein, RS (2004) Defects in cell adhesion and the visceral endoderm following ablation of nonmuscle myosin heavy chain II-A in mice. J. Biol. Chem. 279:41263-6
Abstract	Previous work has shown that ablation or mutation of nonmuscle myosin heavy chain II-B (NMHC II-B) in mice results in defects in the heart and brain with death occurring between embryonic day 14.5 (E14.5) and birth (Tullio, A. N., Accili, D., Ferrans, V. J., Yu, Z. X., Takeda, K., Grinberg, A., Westphal, H., Preston, Y. A., and Adelstein, R. S. (1997) Proc. Natl. Acad. Sci. U. S. A. 94, 12407-12412). 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.
Links	PubMed Online version:10.1074/jbc.C400352200
Keywords	Animals; Cadherins/metabolism; Cell Adhesion/genetics; Cells, Cultured; Cytoskeletal Proteins/metabolism; Endoderm/cytology; Mice; Mice, Knockout; Microscopy, Fluorescence; Myosin Heavy Chains/deficiency; Myosin Heavy Chains/genetics; Myosin Heavy Chains/physiology; Nonmuscle Myosin Type IIA/deficiency; Nonmuscle Myosin Type IIA/genetics; Nonmuscle Myosin Type IIA/physiology; Trans-Activators/metabolism; Viscera/embryology; beta Catenin
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