However, although TepP is required for the recruitment of CrkL and PI3K to nascent inclusions early in infection, their contribution to enhancing bacterial replication, at least in HeLa cells, does not appear to have occurred through interaction with TepP as ΔtepP mutants replicated to levels similar to those seen with wild-type C. trachomatis in cells where Crk and PI3K had been inactivated (Fig. 4). This evidence concerns the gene CRK and infection.