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PLEKHM1 Regulates Salmonella-Containing Vacuole Biogenesis and Infection

McEwan, David G. and Richter, Benjamin and Claudi, Beatrice and Wigge, Christoph and Wild, Philipp and Farhan, Hesso and McGourty, Kieran and Coxon, Fraser P. and Franz-Wachtel, Mirita and Perdu, Bram and Akutsu, Masato and Habermann, Anja and Kirchof, Anja and Helfrich, Miep H. and Odgren, Paul R. and Van Hul, Wim and Frangakis, Achilleas S. and Rajalingam, Krishnaraj and Macek, Boris and Holden, David W. and Bumann, Dirk and Dikic, Ivan. (2015) PLEKHM1 Regulates Salmonella-Containing Vacuole Biogenesis and Infection. Cell Host & Microbe, 17 (1). pp. 58-71.

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Official URL: http://edoc.unibas.ch/dok/A6337537

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Abstract

The host endolysosomal compartment is often manipulated by intracellular bacterial pathogens. Salmonella (Salmonella enterica serovar Typhimurium) secrete numerous effector proteins, including SifA, through a specialized type III secretion system to hijack the host endosomal system and generate the Salmonella-containing vacuole (SCV). To form this replicative niche, Salmonella targets the Rab7 GTPase to recruit host membranes through largely unknown mechanisms. We show that Pleckstrin homology domain-containing protein family member 1 (PLEKHM1), a lysosomal adaptor, is targeted by Salmonella through direct interaction with SifA. By binding the PLEKHM1 PH2 domain, Salmonella utilize a complex containing PLEKHM1, Rab7, and the HOPS tethering complex to mobilize phagolysosomal membranes to the SCV. Depletion of PLEKHM1 causes a profound defect in SCV morphology with multiple bacteria accumulating in enlarged structures and significantly dampens Salmonella proliferation in multiple cell types and mice. Thus, PLEKHM1 provides a critical interface between pathogenic infection and the host endolysosomal system.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Infection Biology > Molecular Microbiology (Bumann)
UniBasel Contributors:Bumann, Dirk
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Cell Press
ISSN:1931-3128
e-ISSN:1934-6069
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:27 Nov 2017 09:47
Deposited On:06 Mar 2015 07:44

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