The large GTPase atlastin controls ER remodeling around a pathogen vacuole.

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.