PTGER3 and coinfection: Experiments in T. brucei have shown that knocking out all of the procyclin genes (Null mutants of GPEET and EP3 on chromosome 6; EP1 and EP2 on chromosome 10) causes no growth defect in vitro and permits completion of the entire life cycle, but causes a selective disadvantage during co-infection with wild type cells in the tsetse fly midgut [51].