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.

Automated summary

A study has found that the microtubule-interacting protein Mllt11 plays an important role in mammalian retinal cell migration. The research shows that the loss of Mllt11 in mouse retinal neuroblasts leads to the abnormal accumulation of ganglion and amacrine cells in the inner nuclear and plexiform layers of the retina.