Taking control: reorganization of the host cytoskeleton by Chlamydia

Abstract

Both actin and microtubules are major cytoskeletal elements in eukaryotic cells that participate in many cellular processes, including cell division and motility, vesicle and organelle movement, and the maintenance of cell shape. Inside its host cell, the human pathogen Chlamydia trachomatis manipulates the cytoskeleton to promote its survival and enhance its pathogenicity. In particular, Chlamydia induces the drastic rearrangement of both actin and microtubules, which is vital for its entry, inclusion structure and development, and host cell exit. As significant progress in Chlamydia genetics has greatly enhanced our understanding of how this pathogen co-opts the host cytoskeleton, we will discuss the machinery used by Chlamydia to coordinate the reorganization of actin and microtubules.

Keywords: ARF; Chlamydia; GTPase; actin; cytoskeleton; microtubules; pathogenicity; post-translational modification.

Figure 1.. Reorganization of the host cytoskeleton during Chlamydia trachomatis infection.

( A) Entry during which a translocated actin-recruiting phosphoprotein (Tarp) induces actin polymerization; ( B) transport of the nascent inclusion to the microtubule-organizing center (MTOC) using CT850; ( C) formation of microtubule cages around the inclusion, in which CT223 is likely involved, and microtubule-dependent movement of lipid droplets (LDs) and multi-vesicular bodies (MVBs) towards the inclusion; ( D) post-translational modifications of microtubule cages and positioning of Golgi mini-stacks around the inclusion controlled by CT813/InaC; ( E) structural scaffolds of actin, septins, and intermediate filaments reinforce the growing inclusion membrane in a CT813-dependent manner; ( F) Chlamydia exits the host cell using CT228-dependent extrusion (left) or through cell lysis (right).