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Salmonella trafficking is defined by continuous dynamic interactions with the endolysosomal system.
Traffic. 2007 Mar; 8(3):212-25
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06 Feb 2007
Controversial
DOI: 10.3410/f.1063745.516668
This manuscript re-examines the ability of the endocytic pathway to function following infection of mammalian cells by Salmonella. Unlike previous reports, these authors find that the Salmonella vacuole maintains communication with incoming endocytic vesicles.
A higher sensitivity, more dynamic approach...Continue reading
A higher sensitivity, more dynamic approach...Continue reading
This manuscript re-examines the ability of the endocytic pathway to function following infection of mammalian cells by Salmonella. Unlike previous reports, these authors find that the Salmonella vacuole maintains communication with incoming endocytic vesicles.
A higher sensitivity, more dynamic approach may have unmasked previously unappreciated trafficking pathways.
A higher sensitivity, more dynamic approach may have unmasked previously unappreciated trafficking pathways.
Disclosures
None declared
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Grinstein S: F1000Prime Recommendation of [Drecktrah D et al., Traffic 2007, 8(3):212-25]. In F1000Prime, 06 Feb 2007; DOI: 10.3410/f.1063745.516668. F1000Prime.com/1063745#eval516668
09 Sep 2011
New Finding, Technical Advance
DOI: 10.3410/f.1063745.14479054
This study establishes that the Salmonella-containing vacuole is able to fuse with the late endocytic compartments. This changes the notion that this bacteria, like a variety of other intracellular bacteria, blocks the maturation of its vacuole at an early stage during infection. Using more-sensitive...Continue reading
This study establishes that the Salmonella-containing vacuole is able to fuse with the late endocytic compartments. This changes the notion that this bacteria, like a variety of other intracellular bacteria, blocks the maturation of its vacuole at an early stage during infection. Using more-sensitive fluid-phase markers, the authors demonstrate that endocytic and lysosomal markers are, in fact, found inside the infectious vacuoles. This study will help shed light on how Salmonella establishes its intracellular niche and what are the requirements for its survival inside the host cell.
Disclosures
None declared
Paumet F: F1000Prime Recommendation of [Drecktrah D et al., Traffic 2007, 8(3):212-25]. In F1000Prime, 09 Sep 2011; DOI: 10.3410/f.1063745.14479054. F1000Prime.com/1063745#eval14479054
F1000Prime Recommendations, Dissents and Comments for [Drecktrah D et al., Traffic 2007, 8(3):212-25]. In F1000Prime, 21 May 2013; F1000Prime.com/1063745
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Following invasion of non-phagocytic host cells, Salmonella enterica survives and replicates within a phagosome-like compartment known as the Salmonella-containing vacuole (SCV). It is now well established that SCV biogenesis, like phagosome biogenesis, involves sequential interactions with the endocytic pathway. However, Salmonella is believed to limit these interactions and, in particular, to avoid fusion of terminal lysosomes with the SCV. In this study, we reassessed this process using a high-resolution live-cell imaging approach and found an unanticipated level of interaction between the SCV and the endocytic pathway. Direct interactions, in which late endosomal/lysosomal content was transferred to SCVs, were detected within 30 min of invasion and continued for several hours. Mechanistically, these interactions were very similar to phagosome-lysosome fusion because they were accompanied by rapid acidification of the SCV, could be blocked by chemical perturbation of microtubules or vacuolar acidification and involved the smallGTPase Rab7. In comparison with vacuoles containing internalized Escherichia coli or heat-killed Salmonella, SCVs did show some delay of fusion and acidification, although, this appeared to be independent of either type III secretion system. These results provide compelling evidence that inhibition of SCV-lysosome fusion is not the major determinant in establishment of the Salmonella replicative niche in epithelial cells.
DOI: 10.1111/j.1600-0854.2006.00529.x
PMID: 17233756
