Rab6 and Rab11 Regulate Chlamydia trachomatis Development and Golgin-84-Dependent Golgi Fragmentation

PLoS Pathogens

Alexander Karlas¹  Charlotte Meissner¹  Dagmar Heuer¹  Anette Rejman Lipinski¹  Thomas F. Meyer¹  Julia Heymann¹  Volker Brinkmann² 

[1] Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany;Microscopy Core Facility, Max Planck Institute for Infection Biology, Berlin, Germany

关键词: Chlamydia infection;    Chlamydia trachomatis;    Chlamydia;    Lipid inclusions;    Small interfering RNAs;    Cell staining;    Luciferase;    Bacterial diseases;   

DOI  :  10.1371/journal.ppat.1000615

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Many intracellular pathogens that replicate in special membrane bound compartments exploit cellular trafficking pathways by targeting small GTPases, including Rab proteins. Members of the Chlamydiaceae recruit a subset of Rab proteins to their inclusions, but the significance of these interactions is uncertain. Using RNA interference, we identified Rab6 and Rab11 as important regulators of Chlamydia infections. Depletion of either Rab6 or Rab11, but not the other Rab proteins tested, decreased the formation of infectious particles. We further examined the interplay between these Rab proteins and the Golgi matrix components golgin-84 and p115 with regard to Chlamydia-induced Golgi fragmentation. Silencing of the Rab proteins blocked Chlamydia-induced and golgin-84 knockdown-stimulated Golgi disruption, whereas Golgi fragmentation was unaffected in p115 depleted cells. Interestingly, p115-induced Golgi fragmentation could rescue Chlamydia propagation in Rab6 and Rab11 knockdown cells. Furthermore, transport of nutrients to Chlamydia, as monitored by BODIPY-Ceramide, was inhibited by Rab6 and Rab11 knockdown. Taken together, our results demonstrate that Rab6 and Rab11 are key regulators of Golgi stability and further support the notion that Chlamydia subverts Golgi structure to enhance its intracellular development.

【 授权许可】

CC BY