Fig. 8.

Model for infection defect of PDEB1 knockout parasites. In wild-type T. brucei (WT), signals in the midgut lumen (black circle) modulate cAMP production (red) by receptor-adenylate cyclases located in specific regions of the flagellum. PDEB1 is distributed along the flagellum (black stars) and restricts cAMP to site of production by the AC, where local changes in cAMP concentration control chemotaxis, group motility or other factors that facilitate traversal of the peritrophic matrix (PM). In the absence of PDEB1 (PDEB1-KO), cAMP levels rise and diffuse through the flagellum and cell, so the parasite is no longer able to generate localized cAMP fluctuations and is thus unable to respond to signals that direct traversal of the PM