Nuclear deformability facilitates apical nuclear migration in the developing zebrafish retina

Nuclear positioning is a crucial aspect of cell and developmental biology. One example is the apical movement of nuclei in neuroepithelia before mitosis, which is essential for proper tissue formation. While the cytoskeletal mechanisms that drive nuclei to the apical side have been explored, the influence of nuclear properties on apical nuclear migration is less understood. Nuclear properties, such as deformability, can be linked to lamin A/C expression levels, as shown in various in vitro studies. Interestingly, many nuclei in early development, including neuroepithelial nuclei, express only low levels of lamin A/C. Therefore, we investigated whether increased lamin A expression in the densely packed zebrafish retinal neuroepithelium affects nuclear deformability and, consequently, migration phenomena. We found that overexpressing lamin A in retinal nuclei increases nuclear stiffness, which in turn indeed impairs apical nuclear migration. Interestingly, nuclei that do not overexpress lamin A but are embedded in a stiffer lamin A-overexpressing environment also exhibit impaired apical nuclear migration, indicating that these effects can be cell non-autonomous. Additionally, in the less crowded hindbrain neuroepithelium, only minor effects on apical nuclear migration are observed. Together, this suggests that the material properties of the nucleus influence nuclear movements in a tissue-dependent manner. [Display omitted] •Lamin A overexpression in zebrafish neuroepithelia increases nuclear stiffness•In retinal neuroepithelia, this leads to hampered nuclear apical migration•Control nuclei migrating in a stiffer environment show impaired apical migration•Migration defects are more significant in densely packed neuroepithelia Maia-Gil et al. probe how nuclear properties affect apical nuclear migration in zebrafish neuroepithelia. Overexpressing lamin A stiffens nuclei, impairing migration. Further, control nuclei in a lamin A-stiffened environment show non-autonomous migration defects, which are tissue-dependent and less prominent in more loosely packed neuroepithelia.