Chlamydia trachomatis Subverts Alpha-Actinins To Stabilize Its Inclusion
Adam Haines, Jordan Wesolowski, Fabienne Paumet
Abstract
Despite antibiotics, recurrent C. trachomatis infections cause significant damage to the genital tract in men and women. Without a preventative vaccine, it is paramount to understand the virulence mechanisms that Chlamydia employs to cause disease. In this context, manipulation of the host cytoskeleton is a critical component of Chlamydia development. Actin scaffolds reinforce the integrity of Chlamydia's infectious vacuole, which is a critical barrier between Chlamydia and the host environment. Having previously established that InaC co-opts RhoA to promote the formation of actin scaffolds around the inclusion, we now show that Chlamydia hijacks a new class of host effectors, α-actinins, to cross-link these scaffolds and further stabilize the inclusion. We also establish that a core function of the chlamydial effector InaC is the regulation of cytoskeletal stability during Chlamydia infection. Ultimately, this work expands our understanding of how bacterial pathogens subvert the actin cytoskeleton by targeting fundamental host effector proteins.