Figure 8.
Hypothetical mechanism of G protein activation during asymmetric cell division. Inscuteable uses its N-terminal “asymmetry domain” to bind to the tetratrico-peptide repeat (TPR) protein Pins. This interaction
facilitates the polarized localization of both Pins and Gαi. Heterotrimeric Gαiβγ binds one or more of the GoLoco motifs present in Pins, causing subunit dissociation and the formation of Inscuteable–Pins–Gαi•GDP and free Gβγ complexes. Dissociated Gβγ and GoLoco-complexed Gαi could possibly regulate independent, as yet uncharacterized, effector pathways to mediate asymmetric cell division.