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Fig. 6. Lack of downregulation of Mitf in Chx10^orJ/orJ retinas predominantly affects H- and D-Mitf. (A) Genetic pathway showing the downregulation of Mitf in the future retina by FGFs emanating from the surface ectoderm (light blue) and Chx10 operating in the distal optic neurepithelium. In Chx10 mutant mice, Mitf is not downregulated in the future retina and the retina hypoproliferates. (B-E) Cryostat sections from E13.5 wild-type (wt) (B,D) and Chx10^orJ/orJ (C,E) eyes labeled for phosphohistone H3 (B,C) or by in situ hybridization using an Mitf exon 1B1b probe (D,E). Note upregulation of exon-1B1b-containing RNA in mutant (E) compared with wild-type (D) retina. Also note that the section in E comes from an embryo with a pigmented RPE (brown stain), whereas the one in D comes from an albino embryo. (F) Limited-cycle RT-PCR analysis performed on RNA isolated from wild-type and Chx10^orJ/orJ whole eyes at E13.5. Primers for A-, J-, H-, D- and M-Mitf are as used for Fig. 3A. For pan-specific amplification, primers in exon 5 and 7 were used. Note that for A- and J-Mitf, at the lower number of PCR cycles the intensities of the bands are slightly increased in mutant compared with wild-type eyes, but at the higher number of cycles the difference is no longer visible. No such differences are seen for M-Mitf. H- and D-Mitf, however, show a clear difference between wild type and mutant at both 29 and 30 cycles of amplification. The use of primers specific for cyclin D1 indicates a reduction in mutant, consistent with the corresponding retinal hypoproliferation.

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