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. 2012 Sep 17;198(6):991–998. doi: 10.1083/jcb.201203083

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© 2012 Chartier et al.

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Figure 4. — Crb controls Rac1 and NADPH oxidase activity and ROS production to maintain retinal integrity. (A–I) Heads from flies maintained under constant illumination (light; A and C–I) or kept in total darkness (dark; B) were fixed, sectioned, and stained for light microscopy analysis. Panels show cross section of a wild-type retina (A), crb mutant (crb−/−) retinas (B and C), crb mutant retina of a fly fed with NSC23766 while submitted to light stress (D), crb mutant retina of a fly raised on a diet containing apocynin (E), crb mutant retina of a fly fed with glutathione (F), crb mutant retina knocked down for Rac1 (G), crb mutant retina in which Nox was knocked down (H), and a Crb knockdown retina in which Sod1 was overexpressed (Sod1 over.; I). Bar, 5 µm. (J) Rhabdomeres were counted on retinal cross sections to quantify the number of surviving photoreceptor cells after 7 d of constant illumination. Reduction of Rac1 activity using NSC23766 or knockdown (Rac1 KD) significantly increased the number of surviving photoreceptor cells in crb mutant retinas. Chemical inhibition of NADPH oxidase using apocynin or knockdown of Nox (Nox KD) had a similar effect. Finally, ROS quenching with glutathione or superoxide detoxification by Sod1 overexpression improved cell fitness in crb mutant or Crb knockdown retinas. Error bars represent the 95% confidence level.