ArticleCellular microbiology2015
Host endoplasmic reticulum COPII proteins control cell-to-cell spread of the bacterial pathogen Listeria monocytogenes.
Article in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The host GTPase Dynamin 2 modulates apical junction structure to control cell-to-cell spread ofInfection and immunity · 2024Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Human Listeriosis.Clinical microbiology reviews · 2023Review
- Listeria monocytogenes Co-Opts the Host Exocyst Complex To Promote Internalin A-Mediated Entry.Infection and immunity · 2022Article
- A targeted approach to investigating immune genes of an iconic Australian marsupial.Molecular ecology · 2022Article
- Article
- The Host GTPase Arf1 and Its Effectors AP1 and PICK1 Stimulate Actin Polymerization and Exocytosis To Promote Entry of Listeria monocytogenes.Infection and immunity · 2020Article
- The Host Scaffolding Protein Filamin A and the Exocyst Complex Control Exocytosis during InlB-Mediated Entry ofInfection and immunity · 2019Article
- Review
- COPII-dependent ER export in animal cells: adaptation and control for diverse cargo.Histochemistry and cell biology · 2018Review
- Actin-based motility and cell-to-cell spread of bacterial pathogens.Current opinion in microbiology · 2017Review
- Recent advances in understandingF1000Research · 2017Review
- Manipulation of host membranes by the bacterial pathogens Listeria, Francisella, Shigella and Yersinia.Seminars in cell & developmental biology · 2016Review
- Bacterial spread from cell to cell: beyond actin-based motility.Trends in microbiology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Listeria monocytogenes is a food-borne pathogen that uses actin-dependent motility to spread between human cells. Cell-to-cell spread involves the formation by motile bacteria of plasma membrane-derived structures termed 'protrusions'. In cultured enterocytes, the secreted Listeria protein InlC promotes protrusion formation by binding and inhibiting the human scaffolding protein Tuba. Here we demonstrate that protrusions are controlled by human COPII components that direct trafficking from the endoplasmic reticulum. Co-precipitation experiments indicated that the COPII proteins Sec31A and Sec13 interact directly with a Src homology 3 domain in Tuba. This interaction was antagonized by InlC. Depletion of Sec31A or Sec13 restored normal protrusion formation to a Listeria mutant lacking inlC, without affecting spread of wild-type bacteria. Genetic impairment of the COPII component Sar1 or treatment of cells with brefeldin A affected protrusions similarly to Sec31A or Sec13 depletion. These findings indicated that InlC relieves a host-mediated restriction of Listeria spread otherwise imposed by COPII. Inhibition of Sec31A, Sec13 or Sar1 or brefeldin A treatment also perturbed the structure of cell-cell junctions. Collectively, these findings demonstrate an important role for COPII in controlling Listeria spread. We propose that COPII may act by delivering host proteins that generate tension at cell junctions.
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