Fig. 9. Overexpression of Six3 and Six3_F88E in the postnatal retina. (A) Postnatal day 0 (P0) retinal progenitor cells were infected with replication incompetent retroviral vectors carrying one of two different forms of the Six3 cDNA upstream of an internal ribosome entry site (IRES) and a human placental alkaline phosphatase reporter gene. LIA-E^Six3 contains the full-length mouse Six3 cDNA. LIA-E^SixF88E contains the full-length Six3 cDNA with the single amino acid substitution (F to E) at position 88. Each retroviral stock (0.5 µl) (LIA-E, LIA-E^Six3 and LIA-E^SixF88E) was injected into the eyes of newborn rats. Three weeks later, the retinae were harvested, stained for alkaline phosphatase expression and sectioned. Clones of cells derived from individual retinal progenitor cells were scored for cell number and cell composition. (B) Normal morphology of photoreceptor cells in LIA-E^SixF88E-infected cells. (C) When the Six3 protein was overexpressed in the developing retinal progenitor cells, nearly 50% of the clones (see Table 1) exhibited an altered photoreceptor phenotype. For simplicity, we have designated this ‘Clone Type A’. Processes were found in the outer nuclear layer similar to rod photoreceptor processes but the outer segments were absent (arrow) and the termini normally associated with rod photoreceptors were malformed (open arrowhead). The cell bodies in these clones tend to lie at the outer nuclear layer/inner nuclear layer boundary. OS, outer segment; ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganglion cell layer. Scale bar: 25 µm.