Fish-derived pluripotent cells instinctively form retinal tissue recapitulating key steps of early eye development.

Cellular and tissue level analysis reveals how different cell behaviors involving dynamics of the basal domain cooperate in space and time to shape an epithelial organ.

High-resolution live imaging analysis shows a constriction mechanism that drives zebrafish optic cup morphogenesis and highlights the role of the extracellular matrix in transmitting tensions beyond the cellular level.

Retinal pigment epithelium flattening is an efficient solution adopted by the fast-developing zebrafish to enable folding of the eye primordia, which contrasts with the proliferation-based mechanism used by amniotes.

A quantitative live imaging approach unveils that earliest neurogenic progenitors in the vertebrate retina arise from asymmetric divisions and that this asymmetry involves Notch signalling through the endocytic pathway.

Par3 is polarized in the plane of the vertebrate neural plate, binds and recruits Prickle3 to the apical membrane and promotes the formation of core planar cell polarity complexes.

A bioengineering approach identifies tissue morphology as an effective variable for controlling the inception of neural organoid morphogenesis via induction of a biomimetic, singular neural rosette tissue cytoarchitecture.

The evolving spatial distribution of nuclei between apical and basal surfaces of the developing retinal neuroepithelium is quantitatively described by a nonlinear diffusion equation accounting for crowding within the tissue.

Comprehensive mouse genetic analyses show, by having mTORC1 constitutively active, a RPC divides and exhausts mitotic capacity faster than neighboring RPCs, and thus produces retinal cells that degenerate with aging-related changes in the mature mouse retina.

The lens-averted domains of the optic vesicle are reservoirs of neuroretinal cells that flow into the developing optic cup in a process that is critically influenced by BMP signaling.