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.

Autophagy
|September 16, 2016
PubMed

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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