Figure 2. Model for agonist-induced trafficking of GPCRs and G proteins.

a. Following the addition of the agonist, a typical GPCR, e.g., β₂-AR, internalizes following a classical endocytic pathway depending on dynamin and clathrin (pink). α_s (green) is enriched in rafts (thick line) and its palmitoylation state is modified (orange). b. α_s internalizes (in some cases α_q, too). This internalization is dependant on cholesterol, a lipid raft constituent (82). The location of α_s after internalization is not clear, maybe diffuse in the cytoplasm or accumulating in small vesicles containing raft markers. GPCR is detected in endosomes. β and γ subunits (blue) also can internalize and would accumulate in vesicles or close to the Golgi. c. The removal of the agonist induces the recycling of GPCR and also α, β and γ subunits to PM. For β₂-AR and a number of other GPCRs, the recycling follows an actin-dependent pathway (red). α_q recycling is dependent on an actin-dependant molecular motor myosin III Ninac and Gβγ in Drosophila photoreceptor cells (56, 115).