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The large GTPase atlastin controls ER remodeling around a pathogen vacuole

Steiner, Bernhard; Weber, Stephen; Kaech, Andres; Ziegler, Urs; Hilbi, Hubert (2018). The large GTPase atlastin controls ER remodeling around a pathogen vacuole. Communicative & Integrative Biology, 11(2):1-5.

Abstract

The ubiquitous environmental bacterium is the causative agent of Legionnaires' pneumonia and replicates in free-living protozoa and mammalian macrophages in a specific compartment, the -containing vacuole (LCV). LCVs communicate with the endosomal, retrograde and secretory vesicle trafficking pathway, and eventually tightly interact with the endoplasmic reticulum (ER). In amoebae and macrophages, the ER tubule-resident large GTPase Sey1/atlastin3 (Atl3) accumulates on LCVs and promotes LCV expansion and intracellular replication of . Fluorescence microscopy of infected with indicated that Sey1 is involved in extensive ER remodeling around LCVs. An ultrastructural analysis confirmed these findings. Moreover, dominant negative Sey1_K154A compromises ER accumulation on LCVs and causes an aberrant ER morphology in uninfected as well as in amoebae infected with avirulent that lack a functional type IV secretion system. Thus, the large, dynamin-like GTPase Sey1/Atl3 controls circumferential ER remodeling during LCV maturation.

Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Medical Microbiology
04 Faculty of Medicine > Center for Microscopy and Image Analysis
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > General Agricultural and Biological Sciences
Language:English
Date:2018
Deposited On:08 Mar 2019 10:47
Last Modified:30 Aug 2024 03:41
Publisher:Taylor & Francis
ISSN:1942-0889
OA Status:Gold
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1080/19420889.2018.1440880
PubMed ID:30083282
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