Figure 1. Retinal Dicer1-deletion leads to lamination defects and RGC degeneration.

Cryosections of heterozygous control (a,c) and mutant (b,d) eyes and subsequent immunohistochemical analysis using anti-GFP (green) antibodies to visualize Cre-positive cells and DAPI counterstain (blue). (a,b) Retinal lamination and thickness are already affected at P0 in Dicer-deleted nasal and temporal retinal areas (b), but EYFP-positive axons coming from nasal and temporal peripheral retina are still present in the fibre layer (arrow) and in the optic nerve (arrowheads). (c,d) Higher magnifications of the optic discs (OD) in control (c) and mutant (d) mice at P8. In contrast to the controls (c), Dicer-negative (EYFP+) RGC axons have disappeared in mutant mice and no longer exit the OD (d). (e,f) Ventral whole-mount view of the optic chiasm (asterisks) under fluorescent illumination after full eye injections of CTB-Alexa-594 and 488 at P8. Wild-type mice show normal sized optic nerves (ON) and optic tracts (OT) (e). In contrast, mice with degenerated nasal and temporal retinal areas exhibit thinner ON and OT, but still forming a normal chiasm at the ventral midline (f). A–P; anterior–posterior; GCL, ganglion cell layer; N–T, nasal–temporal. Scale bar, 200 μm.