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. 2003 May 15;17(10):1225–1239. doi: 10.1101/gad.1081203

Figure 7.

Figure 7

A model for GPR-mediated initiation of G protein signaling. (A) A pathway for spindle force regulation by LIN-5/GPR/Gα, which may be locally regulated by polarity genes. (B) Classical heterotrimeric G protein activation. Exchange of GDP for GTP associated with Gα is stimulated by the guanine nucleotide exchange activity of a GPCR. The heterotrimer is dissociated into two independent signaling modules, Gα·GTP and Gβγ, which are then competent to activate downstream effectors. (C) Activation of G protein signaling in the absence of a GPCR. A GoLoco/GPR motif protein, such as Pins, could compete with and dissociate Gβγ from the heterotrimer, thus initiating Gβγ signaling. It is not known if Gα·GDP/Pins is competent to signal. (D) Receptor-independent initiation of Gα·GTP signaling. The GPR-1/GPR-2 GoLoco proteins could dissociate Gβγ from the heterotrimer and allow the subsequent production of Gα·GTP through the activity of a GEF such as RIC-8. Additionally, free Gβγ could regulate its specific effectors. The signal could be attenuated by intrinsic or GAP-stimulated GTP hydrolysis, allowing for cycling activation of this pathway.