Schematic diagram of RasC-mediated signaling pathways that control chemotaxis. The chemoattractant cAMP signals through the G protein–coupled receptor cAR1 to RasC, leading to TORC2-mediated activation of PKBR1 and PKBA. The activation of PKBA also depends on recruitment to PIP3. Together, the two PKBs phosphorylate a series of substrates and play a critical role in ACA activation, actin polymerization, and chemotaxis. The graphs to the left schematically illustrate the kinetics of G protein α and βγ subunits dissociation, RasC activation, PKB phosphorylation, PKB substrate phosphorylation, and chemotactic responses. The red line shows the typical wild-type responses that are rapidly shut off during persistent stimulation. The green line shows the responses in cells in which the inhibitory signal indicated by (⊥) is bypassed by RasC^Q62L.