The chlamydial organism Simkania negevensis forms ER vacuole contact sites and inhibits ER‐stress |
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Authors: | Adrian Mehlitz Karthika Karunakaran Jo‐Ana Herweg Georg Krohne Sebastian van de Linde Elke Rieck Markus Sauer Thomas Rudel |
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Institution: | 1. University of Wuerzburg, Biocenter, Department of Microbiology, , D‐97074 Wuerzburg, Germany;2. University of Wuerzburg, Biocenter, Division of Electron Microscopy, , D‐97074 Wuerzburg, Germany;3. University of Wuerzburg, Biocenter, Department of Biotechnology and Biophysics, , D‐97074 Wuerzburg, Germany |
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Abstract: | Most intracellular bacterial pathogens reside within membrane‐surrounded host‐derived vacuoles. Few of these bacteria exploit membranes from the host's endoplasmic reticulum (ER) to form a replicative vacuole. Here, we describe the formation of ER–vacuole contact sites as part of the replicative niche of the chlamydial organism Simkania negevensis. Formation of ER–vacuole contact sites is evolutionary conserved in the distantly related protozoan host Acanthamoeba castellanii. Simkania growth is accompanied by mitochondria associating with the Simkania‐containing vacuole (SCV). Super‐resolution microscopy as well as 3D reconstruction from electron micrographs of serial ultra‐thin sections revealed a single vacuolar system forming extensive ER–SCV contact sites on the Simkania vacuolar surface. Simkania infection induced an ER‐stress response, which was later downregulated. Induction of ER‐stress with Thapsigargin or Tunicamycin was strongly inhibited in cells infected with Simkania. Inhibition of ER‐stress was required for inclusion formation and efficient growth, demonstrating a role of ER‐stress in the control of Simkania infection. Thus, Simkania forms extensive ER–SCV contact sites in host species evolutionary as diverse as human and amoeba. Moreover, Simkania is the first bacterial pathogen described to interfere with ER‐stress induced signalling to promote infection. |
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