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Updated: Mar 15, 2026

Use of Shigella flexneri to Study Autophagy-Cytoskeleton Interactions
Published on: September 9, 2014
Mitochondria promote septin assembly into cages that entrap Shigella for autophagy
Sina Krokowski1, Damián Lobato-Márquez1, Serge Mostowy1
1a Section of Microbiology , MRC Centre for Molecular Bacteriology and Infection , Imperial College London , Armstrong Road, London , UK.
Abstract:
Septins are cytoskeletal proteins implicated in cytokinesis and host-pathogen interactions. During macroautophagy/autophagy of Shigella flexneri, septins assemble into cage-like structures to entrap actin-polymerizing bacteria and restrict their dissemination. How septins assemble to entrap bacteria is not fully known. We discovered that mitochondria support septin cage assembly to promote autophagy of Shigella. Consistent with roles for the cytoskeleton in mitochondrial dynamics, we showed that DNM1L/DRP1 (dynamin 1 like) can interact with septins to enhance mitochondrial fission. Remarkably, Shigella fragment mitochondria and escape from septin cage entrapment in order to avoid autophagy. These results uncover a close relationship between mitochondria and septin assembly, and identify a new role for mitochondria in bacterial autophagy.
Insights
Mitochondria aid septin cages in autophagy of Shigella bacteria. Shigella fragments mitochondria to evade this entrapment, revealing a novel role for mitochondria in bacterial autophagy.
Area of Science:
- Cell Biology
- Microbiology
- Immunology
Background:
- Septins are cytoskeletal proteins involved in cell division and host-pathogen interactions.
- Septins form cage-like structures to entrap and facilitate the autophagy of intracellular bacteria like Shigella flexneri.
- The precise mechanisms of septin assembly for bacterial entrapment remain unclear.
Purpose of the Study:
- To investigate the role of mitochondria in septin cage assembly during Shigella autophagy.
- To elucidate the interaction between septins, mitochondria, and bacterial evasion mechanisms.
Main Methods:
- Investigated the interaction between septins and mitochondria during Shigella infection.
- Utilized microscopy and genetic approaches to study mitochondrial dynamics and fission (DNM1L/DRP1).
- Observed bacterial mechanisms for escaping septin entrapment.
Main Results:
- Mitochondria support the assembly of septin cages, promoting the autophagy of Shigella flexneri.
- DNM1L/DRP1 interacts with septins, enhancing mitochondrial fission.
- Shigella flexneri actively fragments mitochondria to escape septin cage entrapment and avoid autophagy.
Conclusions:
- Mitochondria play a crucial role in supporting septin assembly for bacterial autophagy.
- Shigella employs mitochondrial fragmentation as an evasion strategy to prevent its own autophagy.
- This study reveals a novel link between mitochondrial dynamics and host defense against bacterial pathogens.
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