Inducible deletion of Dscam and retinal ganglion cell depletion in Brn3b mutant retinas both indicate that these DSCAM-mediated phenotypes can occur independently.
We also investigated expression of cell-type specific markers in P120 mutant retinas.
Indeed, at 38 hpf, p57kip2 was expressed in large areas of wild-type and p53−/−shh−/− mutant retinas, but absent from the shh−/− mutant retina (Fig. 8C), whereas p53 was much more strongly expressed in the shh−/− mutant retina than in the wild-type and p53−/−shh−/− mutant retinas (Fig. 8C).
The Müller cell-specific Slc38a5 shows significantly reduced transcription level in the LRP5 mutant retinas.
A number of potential target genes are misregulated in Math5 mutant retinas [16].
As melanin amount decreased in Otx2 mutant retinas, we investigated expression of genes involved in its synthesis.
To further characterize the identity of LacZ-positive cells, we isolated Müller cells from 8 days old LRP5−/− mutant retinas.
Since deletion of Otx2 leads to a total loss of photoreceptors in the retina, by comparing expression profiles between the Otx2 CKO retina and control retina, we were able to identify photoreceptor-associated genes more clearly than by using other mutant retinas.
Müller glia, a cell type required to maintain the retinal environment, was present in the wild-type retina at 72 hpf (Fig. 9A-p) but nearly absent in both shh−/− (Fig. 9A-q) and p53−/−shh−/− mutant retinas (Fig. 9A-r).
These data raise the question of whether or not cone cell integration is specifically enhanced in the Gucy2e −/− retinas, or perhaps integrated cells are directed to a cone cell fate by cues in the environment of these mutant retinas (both would increase the cone/rod ratio of integrated cells).
