PUBLICATION
Use of Shigella flexneri to Study Autophagy-Cytoskeleton Interactions
- Authors
- Mazon Moya, M.J., Colucci-Guyon, E., Mostowy, S.
- ID
- ZDB-PUB-140917-1
- Date
- 2014
- Source
- Journal of visualized experiments : JoVE (91): e51601 (Journal)
- Registered Authors
- Colucci-Guyon, Emma, Mostowy, Serge
- Keywords
- none
- MeSH Terms
-
- Animals
- Autophagy/physiology
- Cytoskeleton/microbiology
- Cytoskeleton/pathology
- Dysentery, Bacillary/microbiology*
- Dysentery, Bacillary/pathology
- Female
- Male
- Shigella flexneri/cytology*
- Shigella flexneri/pathogenicity
- Zebrafish
- PubMed
- 25226510 Full text @ J. Vis. Exp.
Citation
Mazon Moya, M.J., Colucci-Guyon, E., Mostowy, S. (2014) Use of Shigella flexneri to Study Autophagy-Cytoskeleton Interactions. Journal of visualized experiments : JoVE. (91):e51601.
Abstract
Shigella flexneri is an intracellular pathogen that can escape from phagosomes to reach the cytosol, and polymerize the host actin cytoskeleton to promote its motility and dissemination. New work has shown that proteins involved in actin-based motility are also linked to autophagy, an intracellular degradation process crucial for cell autonomous immunity. Strikingly, host cells may prevent actin-based motility of S. flexneri by compartmentalizing bacteria inside 'septin cages' and targeting them to autophagy. These observations indicate that a more complete understanding of septins, a family of filamentous GTP-binding proteins, will provide new insights into the process of autophagy. This report describes protocols to monitor autophagy-cytoskeleton interactions caused by S. flexneri in vitro using tissue culture cells and in vivo using zebrafish larvae. These protocols enable investigation of intracellular mechanisms that control bacterial dissemination at the molecular, cellular, and whole organism level.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping