Dynamic Growth and Shrinkage of the Salmonella-Containing Vacuole Determines the Intracellular Pathogen Niche.
SNARE
Salmonella enterica serovar Typhimurium
Salmonella-containing vacuole
compartmental size control
macropinosome
magnetic extraction
membrane rupture
membrane trafficking
proteomics
spacious vacuole-associated tubules (SVAT)
vesicle fusion
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
17 12 2019
17 12 2019
Historique:
received:
03
04
2019
revised:
23
09
2019
accepted:
12
11
2019
entrez:
19
12
2019
pubmed:
19
12
2019
medline:
25
9
2020
Statut:
ppublish
Résumé
Salmonella is a human and animal pathogen that causes gastro-enteric diseases. The key to Salmonella infection is its entry into intestinal epithelial cells, where the bacterium resides within a Salmonella-containing vacuole (SCV). Salmonella entry also induces the formation of empty macropinosomes, distinct from the SCV, in the vicinity of the entering bacteria. A few minutes after its formation, the SCV increases in size through fusions with the surrounding macropinosomes. Salmonella also induces membrane tubules that emanate from the SCV and lead to SCV shrinkage. Here, we show that these antipodal events are utilized by Salmonella to either establish a vacuolar niche or to be released into the cytosol by SCV rupture. We identify the molecular machinery underlying dynamic SCV growth and shrinkage. In particular, the SNARE proteins SNAP25 and STX4 participate in SCV inflation by fusion with macropinosomes. Thus, host compartment size control emerges as a pathogen strategy for intracellular niche regulation.
Identifiants
pubmed: 31851926
pii: S2211-1247(19)31531-1
doi: 10.1016/j.celrep.2019.11.049
pmc: PMC6931108
pii:
doi:
Substances chimiques
Qa-SNARE Proteins
0
SNAP25 protein, human
0
Synaptosomal-Associated Protein 25
0
syntaxin 4, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3958-3973.e7Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.