Planar cell division (PCD) and interkinetic nuclear migration (INM; cell-cycle-dependent local oscillation of nuclei within the developing neuroepithelium) are important for maintaining a neural progenitor pool during neurogenesis. Although the involvement of intracellular components (such as the cytoskeleton and polarity proteins) has been investigated, little was known about the contribution of extracellular cues to these processes. In their study of the medaka fish tacobo (tab) mutant (p. 484), Hiroyuki Takeda and colleagues now reveal that extracellular signals mediated by focal adhesion kinase (FAK) are essential for both PCD and INM during development of the vertebrate nervous system. They identify that the tab locus encodes laminin γ1, and that mutation of this locus causes abnormal PCD and INM in the developing neuroepithelium. Downstream signals of laminin-integrin interactions include FAK; here, the authors find that FAK-mediated signals have a pivitol role in laminin-γ1-dependent morphogenesis by acting in a cell-autonomous manner to regulate localised mitosis, spindle orientation and neurogenesis. Finally, they provide evidence that FAK-mediated signalling cooperates with the dynein motor complex to coordinate these processes in the neural tube.