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Updated: May 22, 2026

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
Published on: October 13, 2015
Retraction of enteropathogenic E. coli type IV pili promotes efficient host cell colonization, effector translocation
Benjamin Aroeti1, Gil Friedman, Efrat Zlotkin-Rivkin
1Department of Cell and Developmental Biology, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem, Israel. aroeti@cc.huji.ac.il
Abstract:
Type IV pili (Tfp) play a primary role in mediating the adherence of pathogenic bacteria to their hosts. The pilus filament can retract with an immense force. However, the role of this activity in microbial pathogenesis has not been rigorously explored. Experiments performed on volunteers suggested that the retraction capacity of enteropathogenic Escherichia coli (EPEC) Tfp is required for full virulence. Here we review our recent study(1) in which we showed that the retraction capacity of the EPEC Tfp facilitates tight-junction disruption and actin-rich pedestal formation by promoting efficient bacterial protein effector translocation into epithelial host cells. We also present new data using live imaging confocal microscopy suggesting that EPEC adheres to monolayers in microcolonies and that Tfp retraction facilitates significant changes in the microcolony shape, which may be critical for efficient effector delivery. Our studies hence suggest novel insights into the role of pili retraction in EPEC pathogenesis.
Insights
Enteropathogenic Escherichia coli (EPEC) uses Type IV pili (Tfp) retraction force to disrupt host cell junctions and form pedestals, enhancing bacterial virulence. This pilus retraction is crucial for efficient effector protein delivery during infection.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Type IV pili (Tfp) are critical for bacterial adherence to host cells.
- The force-generating pilus retraction mechanism is essential for bacterial virulence.
- The precise role of Tfp retraction in enteropathogenic Escherichia coli (EPEC) pathogenesis remains under-investigated.
Purpose of the Study:
- To investigate the role of Tfp retraction in EPEC pathogenesis.
- To elucidate the mechanisms by which Tfp retraction contributes to EPEC virulence.
- To explore the impact of Tfp retraction on host cell interactions and effector delivery.
Main Methods:
- In vivo experiments on volunteers to assess Tfp retraction's role in virulence.
- Live imaging confocal microscopy to observe EPEC adherence and microcolony dynamics.
- Analysis of tight-junction disruption and actin-rich pedestal formation.
Main Results:
- Tfp retraction capacity of EPEC is essential for full virulence.
- Pilus retraction facilitates tight-junction disruption and actin pedestal formation.
- Tfp retraction drives significant changes in EPEC microcolony shape, optimizing effector delivery.
Conclusions:
- Tfp retraction is a key virulence factor for EPEC.
- Efficient effector protein translocation into host cells is mediated by Tfp retraction.
- Pilus retraction dynamics are critical for EPEC pathogenesis and host cell manipulation.
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