Figure 1.

Cartoon depicting the recently identified GPCR-mediated pathways that regulate Dictyostelium chemotaxis. In Dictyostelium chemotaxis is initiated by binding of the chemoattractants to GPCRs, cAR1 (cAMP receptor) and fAR1 (folate receptor), leading to the dissociation of heterotrimeric G protein into Gα2-GTP/Gα4-GTP and a Gβγ dimer. Subsequently, Gα2-GTP, Gα4-GTP and Gβγ all can regulate Ras signaling via Ras specific GEFs. Moreover, Gα2-GTP can directly interact with its effector GflB to activate Rap1, thereby initiating a subset of downstream singling pathways. TORC2 is a common effector of Rap1 and Ras signaling. RasC directly binds the kinase domain of TOR and Rap1 positively regulates the RasC-mediated activation of TORC2 by binding to RIP3, providing a possible mechanism by which TORC2 integrates the Ras and Rap1 pathways during chemotaxis.