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The chlamydial organism S imkania negevensis forms ER vacuole contact sites and inhibits ER ‐stress
Author(s) -
Mehlitz Adrian,
Karunakaran Karthika,
Herweg JoAna,
Krohne Georg,
Linde Sebastian,
Rieck Elke,
Sauer Markus,
Rudel Thomas
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12278
Subject(s) - vacuole , biology , unfolded protein response , endoplasmic reticulum , microbiology and biotechnology , tunicamycin , phagosome , contractile vacuole , autophagy , intracellular , biochemistry , cytoplasm , apoptosis
Summary 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 S imkania negevensis . Formation of ER –vacuole contact sites is evolutionary conserved in the distantly related protozoan host A canthamoeba castellanii . S imkania growth is accompanied by mitochondria associating with the S imkania ‐containing vacuole ( SCV ). Super‐resolution microscopy as well as 3 D reconstruction from electron micrographs of serial ultra‐thin sections revealed a single vacuolar system forming extensive ER – SCV contact sites on the S imkania vacuolar surface. S imkania infection induced an ER ‐stress response, which was later downregulated. Induction of ER ‐stress with T hapsigargin or T unicamycin was strongly inhibited in cells infected with S imkania . Inhibition of ER ‐stress was required for inclusion formation and efficient growth, demonstrating a role of ER ‐stress in the control of S imkania infection. Thus, S imkania forms extensive ER – SCV contact sites in host species evolutionary as diverse as human and amoeba. Moreover, S imkania is the first bacterial pathogen described to interfere with ER ‐stress induced signalling to promote infection.

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