Chlamydia trachomatis (C.t.), the leading cause of bacterial sexually transmitted infections, employs a type III secretion system (T3SS) to translocate two classes of effectors, inclusion membrane proteins and conventional T3SS (cT3SS) effectors, into the host cell to counter host defense mechanisms. Here we employed three assays to directly evaluate secretion during infection, validating secretion for 23 cT3SS effectors. As bioinformatic analyses have been largely unrevealing, we conducted affinity purification-mass spectrometry to identify host targets and gain insights into the functions of these effectors, identifying high confidence interacting partners for 21 cT3SS effectors. We demonstrate that CebN localizes to the nuclear envelope in infected and bystander cells where it interacts with multiple nucleoporins and Rae1, blocking STAT1 nuclear import following IFN-γ stimulation. By building a cT3SS effector-host interactome, we have identified novel pathways that are targeted during bacterial infection and have begun to address how C.t. effectors combat cell autonomous immunity.
性别传播感染的主要原因是沙丘菌(C.T. IOINFORMITIC分析已经Largely unrevealing, we conducted affinity purification-mass spectrometry to identify host targets and gain insights into the functions of these effects, identifying high confidence interacting partners for 21 cT3SS effects. We demonstrate that CebN localizes to the nuclear envelope in infected and bystander cells where it interacts with multiple nuclear nucleoporins and Rae1, blocking STAT1 nuclear import following IFN-γ stimulation. By building a cT3SS effector-host相互作用,我们已经确定了在细菌感染过程中针对的新型途径,并开始解决C.T的作用。