Open AccessThe COPII complex and lysosomal VAMP 7 determine intracellular Salmonella localization and growth
Author(s) -
Santos José Carlos,
Duchateau Magalie,
Fredlund Jennifer,
Weiner Allon,
Mallet Adeline,
Schmitt Christine,
Matondo Mariette,
Hourdel Véronique,
ChamotRooke Julia,
Enninga Jost
Publication year - 2015
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12475
Subject(s) - vacuole , biology , endoplasmic reticulum , copii , intracellular , microbiology and biotechnology , salmonella , cytosol , vesicle , organelle , lysosome , intracellular parasite , bacteria , secretory pathway , cytoplasm , golgi apparatus , biochemistry , membrane , genetics , enzyme
Summary S almonella invades epithelial cells and survives within a membrane‐bound compartment, the S almonella ‐containing vacuole ( SCV ). We isolated and determined the host protein composition of the SCV at 30 min and 3 h of infection to identify and characterize novel regulators of intracellular bacterial localization and growth. Quantitation of the SCV protein content revealed 392 host proteins specifically enriched at SCV s, out of which 173 associated exclusively with early SCV s, 124 with maturing SCV and 95 proteins during both time‐points. V acuole interactions with endoplasmic reticulum‐derived coat protein complex II vesicles modulate early steps of SCV maturation, promoting SCV rupture and bacterial hyper‐replication within the host cytosol. On the other hand, SCV interactions with VAMP 7‐positive lysosome‐like vesicles promote S almonella ‐induced filament formation and bacterial growth within the late SCV . Our results reveal that the dynamic communication between the SCV and distinct host organelles affects both intracellular S almonella localization and growth at successive steps of host cell invasion.