Elevated Rh1 levels are responsible for PR loss in the <i>fatp</i> mutant.

<p>(A) Western blot analysis of Rh1 in boiled head extracts from control, <i>fatp^{k10307/k10307}</i>, <i>rh1^G69D/+</i> and <i>fatp^{k10307/k10307}</i>/<i>rh1^G69D/+</i> 1 to 11-day-old flies. Tubulin was used as a loading control. (B) Quantification of protein levels. Dimer and oligomer forms of Rh1 were due to the boiling of the extracts. Rh1 levels were twofold higher in the <i>fatp</i> mutant than in the control. The level of Rh1 was substantially lower in the <i>rh1^G69D/+</i> single mutant and in the <i>fatp^{k10307/k10307}</i>/<i>rh1^G69D/+</i> double mutant. (C) Western blot analysis of Rh1 and tubulin in <i>fatp</i> mutant mosaic retina extracts from 5-day-old flies reared from the embryonic stage on control (+VitA) and vitamin A-deficient (-VitA) media. Tubulin was used as a loading control. Rh1 was not detectable in flies reared on vitamin A-deficient medium. (D, E) Visualization of <i>fatp</i> mutant mosaic retina of 5-day-old flies reared from the embryonic stage on control (D) and vitamin A-deficient (E) media using the Tomato/GFP-FLP/FRT method (scale bar = 10 µm). (F) Quantification of mutant PR loss (t-test, n≥12). <i>fatp</i> mutant PR viability was dramatically restored in flies reared on vitamin A-deficient medium. (G–J) Analysis of the loss of <i>fatp^k10307</i>, <i>fatp^k10307 arr2^3/+</i> and <i>fatp^k10307 arr2^3/3</i> double mutant PRs using resin-embedded tangential sections in 34-day-old flies (scale bar = 10 µm). (H) Quantification of PR loss. In the double mutants retinas, PRs were significantly rescued (p = 0.0021 and p = 0.0016, t-test, n = 6).