Retinal neuroblast migration and ganglion cell layer organization require the cytoskeletal‐interacting protein Mllt11.

Background: The vertebrate retina is an organized laminar structure comprised of distinct cell types populating three nuclear layers. During development, each retinal cell type follows a stereotypical temporal order of genesis, differentiation, and migration, giving rise to its stratified organization. Once born, the precise positioning of cells along the apico‐basal (radial) axis of the retina is critical for subsequent connections to form, relying on highly orchestrated migratory processes. While these processes are critical for visual function to arise, the regulators of cellular migration and retinal lamination remain largely unexplored. Results: We report a role for a microtubule‐interacting protein, Mllt11 (myeloid/lymphoid or mixed‐lineage leukemia; translocated to chromosome 11/All1 fused gene from chromosome 1q) in mammalian retinal cell migration during retinogenesis. We show that Mllt11 loss‐of‐function in mouse retinal neuroblasts affected the migration of ganglion and amacrine cells into the ganglion cell layer and led to their aberrant accumulation in the inner nuclear and plexiform layers. Conclusions: We demonstrate a role for Mllt11 in neuroblast migration and formation of the ganglion cell layer of the retina. Key Findings: Mllt11 plays a role in mammalian retinal lamination during development.Mllt11 regulates neuroblast morphology important for migration into the ganglion cell layer.Mllt11 loss of function leads to aberrant accumulation of retinal ganglion cells and displaced amacrine cells in the inner plexiform layer. [ABSTRACT FROM AUTHOR]