Journal
EMBO REPORTS
Volume 18, Issue 10, Pages 1817-1836Publisher
WILEY
DOI: 10.15252/embr.201743903
Keywords
Dictyostelium discoideum; macrophage; pathogen vacuole; phosphoinositide lipid; type IV secretion
Categories
Funding
- Institute of Medical Microbiology UZH
- Swiss National Science Foundation (SNF) [31003A_153200]
- Novartis Foundation for Medical-Biological Research
- OPO Foundation
- German Bundesministerium fur Bildung und Forschung (BMBF) [031A410A]
- Swedish Research Council [2014-396]
- SNF Ambizione fellowship
Ask authors/readers for more resources
The pathogenic bacterium Legionella pneumophila replicates in host cells within a distinct ER-associated compartment termed the Legionella-containing vacuole (LCV). How the dynamic ER network contributes to pathogen proliferation within the nascent LCV remains elusive. A proteomic analysis of purified LCVs identified the ER tubule-resident large GTPase atlastin3 (Atl3, yeast Sey1p) and the reticulon protein Rtn4 as conserved LCV host components. Here, we report that Sey1/Atl3 and Rtn4 localize to early LCVs and are critical for pathogen vacuole formation. Sey1 overproduction promotes intracellular growth of L. pneumophila, whereas a catalytically inactive, dominant-negative GTPase mutant protein, or Atl3 depletion, restricts pathogen replication and impairs LCV maturation. Sey1 is not required for initial recruitment of ER to PtdIns(4)P-positive LCVs but for subsequent pathogen vacuole expansion. GTP (but not GDP) catalyzes the Sey1-dependent aggregation of purified, ER-positive LCVs in vitro. Thus, Sey1/Atl3-dependent ER remodeling contributes to LCV maturation and intracellular replication of L. pneumophila.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available