Abstract

Adherens junctions (AJs) comprise cell-cell adhesion complexes that are organized as belt-like structures at the most apical-lateral plasma membrane. In embryonic neural stem and progenitor cells (NSPCs), these junctional complexes are essential for the maintenance of the ventricular lining and the cerebral cytoarchitecture. Several reports in humans and animal models have shown that loss of function of proteins involved in the assembly and/or turnover of AJs components gives rise to a phenotype characterized by disruption of the ventricular zone, increased cell death, and defective corticogenesis. In turn, these models consistently replicate a wide range of defects expressed by vertical transmission of Zika virus (ZIKV), a flavivirus with a high tropism by neural tissues. This chapter summarizes relevant aspects of the structure and function of AJs during brain development, as well as provides novel insights that may contribute to the current knowledge about the etiopathogenesis of congenital ZIKV syndrome (CZS)