Chlamydia trachomatis infection prevents front-rear polarity of migrating HeLa cells.
Chlamydiae are obligate intracellular bacterial pathogens that cause trachoma, sexually transmitted diseases and respiratory infections in humans. Fragmentation of the host cell Golgi apparatus (GA) is essential for chlamydial development, whereas the consequences for host cell functions, including cell migration are not well understood. We could show that Chlamydia trachomatis-infected cells display decelerated migration and fail to repopulate monolayer scratch wounds. Furthermore, infected cells lost the ability to reorient the fragmented GA or the microtubule organization centre (MTOC) after a migratory stimulus. Silencing of golgin-84 phenocopied this defect in the absence of the infection. Interestingly, GA stabilization via knockdown of Rab6A and Rab11A improved its reorientation in infected cells and it was fully rescued after inhibition of Golgi fragmentation with WEHD-fmk. These results show that C. trachomatis infection perturbs host cell migration on multiple levels, including the alignment of GA and MTOC.
Robert Koch-Institute, Junior Research Group 5 Sexually Transmitted Bacterial Pathogens, Nordufer 20, 13353, Berlin, Germany.
Julia
J
Heymann
Anette
A
Rejman Lipinski
Bianca
B
Bauer
Thomas F
TF
Meyer
Dagmar
D
Heuer
D002465:Cell Movement; D016764:Cell Polarity; D002692:Chlamydia trachomatis / Q000472:pathogenicity*; D004847:Epithelial Cells / Q000382:microbiology* / Q000502:physiology*; D006056:Golgi Apparatus / Q000378:metabolism; D006367:HeLa Cells; D054884:Host-Pathogen Interactions; D006801:Humans; D008870:Microtubules / Q000378:metabolism