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Fig. 4. Absence of programmed cell death of Brn3b-null RGCs in Brn3a^ki knock-in mice during embryonic development. Cryosections of retinas at E13.5 to P0 were stained with X-Gal to reveal the RGCs by the expression of Brn3b-lacZ reporter gene at Brn3b locus. (A,D,G,J) Control heterozygous Brn3b^lacZ/+ mice. During retinal development, RGCs are generated and remained in the GCL. (B,E,H,K) Brn3b^lacZ/AP mice. The lacZ-expressing RGCs were initially formed normally in the GCL (E) but a majority of them degenerated before birth (E,H,K). (C,F,I,L) Brn3b^3a/lacZ mice. Replacement of Brn3b with Brn3a^ki prevents the apoptosis of Brn3b-null RGCs marked by the strong X-Gal staining in the GCL. RPE, retinal pigmented epithelium; NBL, neuroblast layer; GCL, ganglion cell layer; l, lens. Scale bar: 100 µm.

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