Vinculin is required for interkinetic nuclear migration (INM) and cell cycle progression

Vinculin is an actin-binding protein (ABP) that strengthens the connection between the actin cytoskeleton and adhesion complexes. It binds to beta-catenin/N-cadherin complexes in apical adherens junctions (AJs), which maintain cell-to-cell adhesions, and to talin/integrins in the focal adhesions (FAs) that attach cells to the basal membrane. Here, we demonstrate that beta-catenin targets vinculin to the apical AJs and the centrosome in the embryonic neural tube (NT). Suppression of vinculin slows down the basal-to-apical part of interkinetic nuclear migration (BA(INM)), arrests neural stem cells (NSCs) in the G2 phase of the cell cycle, and ultimately dismantles the apical actin cytoskeleton. In the NSCs, mitosis initiates when an internalized centrosome gathers with the nucleus during BA(INM). Notably, our results show that the first centrosome to be internalized is the daughter centrosome, where beta-catenin and vinculin accumulate, and that vinculin suppression prevents centrosome internalization. Thus, we propose that vinculin links AJs, the centrosome, and the actin cytoskeleton where actomyosin contraction forces are required.

Automated summary

Vinculin is an actin-binding protein that plays a crucial role in cell adhesion and cytoskeleton connection. Beta-catenin targets vinculin to the apical adherens junctions and centrosome in the embryonic neural tube. Suppression of vinculin affects neural stem cell division and disrupts the integrity of the cell cytoskeleton.