The chlamydial organism Simkania negevensis forms ER vacuole contact sites and inhibits ER‐stress. (21st March 2014)

• Record Type: Journal Article
• Authors: Mehlitz, Adrian; Karunakaran, Karthika; Herweg, Jo‐Ana; Krohne, Georg; van de Linde, Sebastian; Rieck, Elke; Sauer, Markus; Rudel, Thomas
• Is Part Of: Cellular microbiology. Volume 16:Number 8(2014:Aug.)
• Page Start: 1224
• Page End: 1243
• Publication Date: 2014-03-21
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12278
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>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 <italic>S</italic><italic>imkania negevensis</italic>. Formation of ER–vacuole contact sites is evolutionary conserved in the distantly related protozoan host <italic>A</italic><italic>canthamoeba castellanii</italic>. <italic>S</italic><italic>imkania</italic> growth is accompanied by mitochondria associating with the <italic>S</italic><italic>imkania</italic>‐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 <italic>S</italic><italic>imkania</italic> vacuolar surface. <italic>S</italic><italic>imkania</italic> 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 <italic>S</italic><italic>imkania</italic>. Inhibition of ER‐stress was required for inclusion formation and efficient growth, demonstrating a role of ER‐stress in the control of <italic>S</italic><italic>imkania</italic> infection. Thus, <italic>S</italic><italic>imkania</italic> forms extensive ER–SCV contact sites in host species evolutionary as diverse as human and amoeba. Moreover, <italic>S</italic><italic>imkania</italic> is the first bacterial pathogen described to interfere with ER‐stress induced signalling to promote infection.</p> </abstract>