Fig 4.

Disruption of inclusion microdomains is not linked to an augmented cell-autonomous defense. (A) Co-IP reveals a differential ability of CpoS variants to interact with IPAM. HeLa cells were co-infected with CTL2/pIPAM(L2)-MYC and derivatives of CTL2-cpoS::cat expressing variants of CpoS-FLAG (2.5 IFU/cell each). CpoS-FLAG constructs were precipitated from lysates at 26 hpi. Eluates were analyzed by western blot analysis (* indicates visible Co-IP of IPAM(L2)-MYC). (B) Localization of IPAM in infected HeLa cells (5 IFU/cell, 20 hpi, scale = 20 µm, confocal). (C) Chlamydia’s ability to dampen cell death and IFN responses does not depend on IPAM. Luciferase activity in A2EN-ISRE reporter cells (2.5 IFU/cell, 14 hpi) and cell death in A2EN and HeLa cells (2.5 IFU/cell, 24 hpi) (mean ± SD, n = 3–7, one-way ANOVA: indicated are significant differences compared to CTL2).