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. 2009 Aug 12;4(8):e6616. doi: 10.1371/journal.pone.0006616

Figure 6. Disruption of Pro-apoptotic Bax Was Sufficient to Prevent Rod Photoreceptor Defect and Loss in Rpe65-deficient Animals.

Figure 6

(A) Examination of retinal morphology (600×) and (C) counting rows of rod nuclei at 6 months (6 m) of age showed that whereas ONL thickness was reduced in Rpe65−/− retinas, loss of photoreceptor nuclei was prevented in Rpe65-deficient retinas lacking Bax. The data presented are the mean±SE of four independent experiments. # p<0.01 by ANOVA test for Rpe65−/− versus wt; ## p<0.05 by ANOVA test for Rpe65−/− versus Rpe65−/−/Bax−/−. (B) Histological analysis at 12 months (12 m) of age showing long-term protection of ONL and OS integrity in the absence of pro-apoptotic Bax in Rpe65−/−/Bax−/− mice. ONL, outer nuclear layer; INL, inner nuclear layer; IS, inner segment; OS, outer segment.