Nonmuscle myosin II isoform and domain specificity during early mouse development

摘要: Nonmuscle myosins (NMs) II-A and II-B are essential for embryonic mouse development, but their specific roles not completely defined. Here we examine the isoforms domain specifically in vivo vitro by studying mice cells which nonmuscle myosin heavy chain (NMHC) is genetically replaced NMHC or chimeric IIs that exchange rod head domains of NM II-B. In contrast with failure visceral endoderm formation resulting day (E)6.5 lethality A−/A− mice, replacement restores a normal endoderm. This finding consistent II's role cell adhesion also confirms an essential, isoform-independent requirement II function. The knock-in die between E9.5 12.5 because defects placenta associated abnormal angiogenesis migration, revealing unique function development. results further support directed migration focal formation. These findings demonstrate isoform-specific during these processes, making another isoform, isoforms, less successful. substitutions only related to different kinetic properties II-B, subcellular localization determined C-terminal domain. highlight functions N-terminal motor cell-cell cell-matrix adhesion.