Figure 5.

Dynein is important for Rh1 and Eys trafficking. RNAi line BDSC 36583 (Dhc64C-RNAi) was used to deplete Dhc64c. Dhc64C-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 dynein (Dhc64c) deficient retinas. We categorized this defect as Class I. (B) TEM analysis revealed a smaller IRS, smaller rhabdomeres, bloated PRCs (arrow) and cytoplasmic accumulation of vesicles (arrowheads) in dynein deficient retinas. (C) Dynein deficient PRCs showed cytoplasmic accumulation of Rh1 and Eys (arrowheads). Cytoplasmic Eys colocalized with cytoplasmic Rh1. (D) Levels or localization of Crb was normal in Dhc64c depleted PRCs. Arrowhead points to cytoplasmic accumulation of Eys. (E) Levels/localization of the basolateral protein Nrv (K⁺Na⁺ATPase subunit) was not affected by dynein depletion. Acti-stain555 (F-actin) was used to visualize the rhabdomeres. (F) IRS size was significantly reduced in dynein compromised retinas. A total of 106 individual IRS were measured for control and 109 for dynein deficient ommatidia using 3 different animals per genotype. Values were normalized to the control. Error bars represent standard deviation. Unpaired non-parametric Mann-Whitney test. (G) Summary model indicating the secretion of Rh1 and Eys containing secretory vesicles depends on dynein and that secretion of Rh1, Eys, and Crb requires kinesin function (see Figures S2 and S4). See Figure 1A for annotation and text for discussion.