Figure 6.

Syx7/Avl deficient PRCs show enhanced surface levels of Rh1, Eys and Crb. RNAi line BDSC 29546 (Syx7-RNAi) was used to deplete Syx7/Avl. Syx7-RNAi was crossed with UAS-dicer-2; pGMR-Gal4. UAS-dicer-2/+; pGMR-Gal4/+ was used as control. Scale bars, 5 μm. (A) Individual rhabdomeres were partially visible in Syx7/Avl deficient retinas. We categorized this defect as Class I. (B) Knockdown of Syx7/Avl led to rhabdomeral fragmentation and degeneration. (C) Syx7/Avl deficient PRCs show increased apical and basolateral accumulation of Rh1. (D) IRS area stained with Eys and stalk membranes labeled with Crb are larger in Syx7/Avl deficient PRCs compared to the control. (E) Levels/localization of the basolateral protein Nrv (K⁺Na⁺ATPase subunit) is normal in Syx7/Avl deficient PRCs. Acti-stain555 (F-actin) was used to visualize rhabdomeres which appear disorganized. (F) IRS size was significantly larger in Syx7/Avl deficient retinas compared to controls. A total of 69 individual IRS were measured for the control and 138 for Syx7/Avl knockdown PRCs using 3 different animals per genotype. Values were normalized to the control. Error bars represent standard deviation. Unpaired non-parametric Mann-Whitney test. (G) Stalk membranes were significantly larger in Syx7Avl deficient PRCs compared to controls. A total of 182 individual stalk membranes were measured for the control and 126 for Syx7/Avl deficient knockdown PRCs. Error bars represent standard deviation. Unpaired non-parametric Mann-Whitney test. (H) Summary model indicating that the endocytosis of Rh1, Crb, and Eys depends on Syx7/Avl. See Figure 1A for annotation and text for discussion.