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. 2008 Dec 10;28(50):13684–13695. doi: 10.1523/JNEUROSCI.4333-08.2008

Figure 3.

Figure 3.

Transgenic expression of Nok in the RPE of pt106 is sufficient to rescue the patchy RPE defect caused by the nokm520 mutation. A–F, The expression of transgenic Nok in pt106 (E, F) restores the RPE integrity to a level indistinguishable from that of wild-type (WT) RPE (A, B). The phenotypes of a curled body axis and a paracardiac edema are still present in pt106 (E) as in nokm520 mutants (C) at 36 hpf. B, D, and F show magnified eye regions in A, C, and E, respectively. G, H, Anti-Nok547–703 antibody visualized peripheral localization of transgenic Nok (red) in the eyes of pt106 at 33 hpf (arrows). G and H show images of the same embryo at different confocal optical sections. The inset shows a magnified RPE area that expresses transgenic Nok (red). I–K, Transgenic Nok (red; arrows) localizes to the RPE that was visualized with RPE-specific marker zpr2 (green) at 72 hpf. The arrowhead indicates the nonspecific staining of the anti-Nok547–703 antibody (Fig. 2). I shows the overview of an entire eye. L, M, Using a GFP riboprobe that recognizes the mRNA of the transgenic nok gene but not the endogenous nok gene (Fig. 2), an in situ hybridization analysis of 33 hpf PTU-treated wild-type pt106bing-33 embryos confirmed that the transgene is expressed in the RPE (arrows) but not in the neural retina (L). A control regular wild-type embryo showed no detectable signal (M).