The cell autonomous immune defense against Chlamydia

The inclusion membrane acts as the Chlamydia-host interface. Chlamydia trachomatis secretes various bacterial effector proteins that integrate into the inclusion membrane. These effectors interfere with host cell trafficking and signalling pathways to maintain their replicative niche of Chlamydia. One of these effectors is the deubiquitinating enzymes  Chlamydial deubiquitinase (Cdu)-1, secreted into the inclusion membrane during infection with its catalytically active site facing the host cell’s cytosol. From there, Cdu1 mediates host cell survival and protects chlamydial inclusions from ubiquitination as well as the recruitment of the autophagy machinery. We could also show that Cdu1 influences the redistribution of the Golgi around the inclusion, a phenotype which is associated with the uptake of host cell lipids. As a part of the Research and Training Group GRK 2243, we investigate the role of ubiquitination during chlamydial infection. We aim to understand the interactions of Cdu1 with host cell pathways, that mediate chlamydial intracellular survival and successful replication.