Fig. 8.

Proposed role of PIP4K in regulating endocytic turnover of Rh1. Rhodopsin (R) is activated by light to metarhodopsin (M*), which triggers GPCR activation and, in turn, causes PLC-mediated PIP₂ turnover in the rhabdomere/apical plasma membrane of fly PRs. M* is bound by arrestin proteins (Arr) and endocytosed by CME. PIP4K regulates CME from the plasma membrane, and its absence causes increased CME uptake, leading to an increased number of Rhodopsin-loaded early endocytic vesicles (RLVs) that undergo homotypic fusion to form larger early endocytic compartments, and later mature normally as enlarged late endosomes and MVBs. RE, recycling endosomes.