ArticleInfection and immunity2014
The serine/threonine kinase STK11 promotes Shigella flexneri dissemination through establishment of cell-cell contacts competent for tyrosine kinase signaling.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Identification, antimicrobial susceptibility test, and pathogenicity analysis ofFrontiers in microbiology · 2026Article
- Article
- Host PIK3C3 promotes Shigella flexneri spread from cell to cell through vacuole formation.PLoS pathogens · 2025Article
- ThemBio · 2025Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Invading Bacterial Pathogens Activate Transcription Factor EB in Epithelial Cells through the Amino Acid Starvation Pathway of mTORC1 Inhibition.Molecular and cellular biology · 2022Article
- The type 3 secretion effector IpgD promotes S. flexneri dissemination.PLoS pathogens · 2022Article
- The type three secretion system effector protein IpgB1 promotes Shigella flexneri cell-to-cell spread through double-membrane vacuole escape.PLoS pathogens · 2022Article
- Neisseria gonorrhoeae subverts formin-dependent actin polymerization to colonize human macrophages.PLoS pathogens · 2021Article
- Lewis Blood-group Antigens Are Associated With Altered Susceptibility to Shigellosis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- Host Genome-Wide Association Study of Infant Susceptibility toInfection and immunity · 2021Article
- Mechanisms of bacillary dysentery: lessons learnt from infant rabbits.Gut microbes · 2020Review
- Critical role of bacterial dissemination in an infant rabbit model of bacillary dysentery.Nature communications · 2019Article
- Principles of intracellular bacterial pathogen spread from cell to cell.PLoS pathogens · 2018Review
- Spatial, Temporal, and Functional Assessment of LC3-Dependent Autophagy in Shigella flexneri Dissemination.Infection and immunity · 2018Article
- Article
- Actin-based motility and cell-to-cell spread of bacterial pathogens.Current opinion in microbiology · 2017Review
- Implications of Spatiotemporal Regulation of Shigella flexneri Type Three Secretion Activity on Effector Functions: Think Globally, Act Locally.Frontiers in cellular and infection microbiology · 2016Review
- Cellular Aspects of Shigella Pathogenesis: Focus on the Manipulation of Host Cell Processes.Frontiers in cellular and infection microbiology · 2016Review
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2 authors.
Funding
Abstract
Shigella flexneri is an intracellular pathogen that disseminates in the intestinal epithelium by displaying actin-based motility. We found that although S. flexneri displayed comparable actin-based motilities in the cytosols of HeLa229 and HT-29 epithelial cell lines, the overall dissemination process was much more efficient in HT-29 cells. Time-lapse microscopy demonstrated that as motile bacteria reached the cell cortex in HT-29 cells, they formed membrane protrusions that resolved into vacuoles, from which the bacteria escaped and gained access to the cytosol of adjacent cells. In HeLa229 cells, S. flexneri also formed membrane protrusions that extended into adjacent cells, but the protrusions rarely resolved into vacuoles. Instead, the formed protrusions collapsed and retracted, bringing the bacteria back to the cytosol of the primary infected cells. Silencing the serine/threonine kinase STK11 (also known as LKB1) in HT-29 cells decreased the efficiency of protrusion resolution into vacuoles. Conversely, expressing STK11 in HeLa229 cells, which lack the STK11 locus, dramatically increased the efficiency of protrusion resolution into vacuoles. S. flexneri dissemination in HT-29 cells led to the local phosphorylation of tyrosine residues in protrusions, a signaling event that was not observed in HeLa229 cells but was restored in STK11-expressing HeLa229 cells. Treatment of HT-29 cells with the tyrosine kinase inhibitor imatinib abrogated tyrosine kinase signaling in protrusions, which correlated with a severe decrease in the efficiency of protrusion resolution into vacuoles. We suggest that the formation of STK11-dependent lateral cell-cell contacts competent for tyrosine kinase signaling promotes S. flexneri dissemination in epithelial cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.