Early in retinal development, neuroepithelial progenitor cells begin to divide in a neurogenic mode in which at least one daughter cell exits the cell cycle and differentiates into a neuron. Now, on , Brian Link and colleagues investigate the cell biological mechanisms that influence neurogenesis by analysing zebrafish and mouse retinal neuroepithelia deficient for Llgl1 (lethal giant larval protein homologue 1), a protein that is implicated in apicobasal polarity, asymmetric division, cell shape and cell-cycle exit. The researchers show that Llgl1-deficient neuroepithelia retain apicobasal polarity but have expanded apical domains. Importantly, Llgl1-deficient neuroepithelia display increased Notch activity and reduced neurogenesis. Expansion of the apical domain through inhibition of Shroom3 also increases Notch activity and reduces neurogenesis. These results, together with studies of interkinetic nuclear migration (the apical-to-basal movement of neuroepithelial nuclei that is linked with cell-cycle exit) in Llgl1-depleted retinal precursors, suggest that the size of the apical domain of retinal neuroepithelia modulates the strength of the polarised signals that influence neurogenesis.
