We first examined the retinal architecture in conditional trans-heterozygous and Pcdhg null mutant animals. Retina lamination was normal and the ONL and OPL layers were unaffected in all three types of mutants. However, while the INL and IPL layers in Pcdhgfcon3/tako mutant retinas were indistinguishable from those in control, they were significantly thinner in both Pcdhgfcon3//tcko and Pcdhgfcon3/fcon3 mutant retinas (Figures 3A-A”’, 3D). Quantification of retina interneurons using cell-type specific markers revealed that INL thinning in Pcdhgfcon3//tcko mutants is due to reduced numbers of bipolar (Chx10+) and amacrine (Pax6+) interneurons (Figures 3B-B”’, 3E) as in the null (Lefebvre et al., 2008). Likewise, the loss of RGC projection neurons (Brn3a+) in Pcdhgfcon3/tcko trans-heterozygous retinas is equal in severity to that of Pcdhgfcon3/fcon3 mutants (Figures 3C-C”’, 3F). By contrast, we found no change in retina cell number in conditional Pcdhgfcon3/tako trans-heterozygous retinas (Figures 3D–F). Like the 3 C-type genes, the 3 A-type genes are also expressed in these cell types in the developing retina (Figures S3A-B), indicating that the full spectrum of Pcdhg isoforms are not required for neuronal survival. Increased levels
