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

• Published in: The Journal of cell biology Vol. 223; no. 1; p. 1
• Main Authors: Ochoa, Andrea, Herrera, Antonio, Menendez, Anghara, Estefanell, María, Ramos, Carlota, Pons, Sebastian
• Format: Journal Article
• Language: English
• Published: New York Rockefeller University Press 01-01-2024
• Subjects: Actin; Actomyosin; Adherens junctions; Cell cycle; Cell Cycle and Division; Cell migration; Cytoskeleton; Development; G2 phase; Integrins; Internalization; Mitosis; N-Cadherin; Neural stem cells; Neural tube; Neuroscience; Stem cells; Talin; Vinculin; β-Catenin
• ISSN: 0021-9525; 1540-8140
• DOI: 10.1083/jcb.202106169

Vinculin is an actin-binding protein (ABP) that strengthens the connection between the actin cytoskeleton and adhesion complexes. It binds to β-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 β-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 (BAINM), 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 BAINM. Notably, our results show that the first centrosome to be internalized is the daughter centrosome, where β-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.