FIG 4.

Model for cAMP microdomain regulation of social motility. (A) Schematic model for AC6-dependent control of social motility in wild-type cells (WT) and AC6 knockdown or catalytic mutant cells [AC6(−)]. AC6 is one of several ACs in the trypanosome flagellum. The model posits that ACs recognize different ligands, depending on their divergent extracellular domains, and that ligand binding regulates AC activity. cAMP produced specifically by AC6 acts to inhibit social motility, and when AC6 activity is reduced through ligand-mediated regulation (WT), this results in reduced cAMP and activation of social motility. Constitutive inactivation of AC6, e.g., through knockdown or expression of a catalytic mutant [AC6(−)], causes a signal-independent decrease in local cAMP, resulting in a precocious, hypersocial phenotype. (B) Reciprocal relationship between social motility (SoMo) and cAMP concentration.