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Legionella blocks autophagy by cleaving STX17 (syntaxin 17)
Kohei Arasaki1, Mitsuo Tagaya1
1a School of Life Sciences , Tokyo University of Pharmacy and Life Sciences , Hachioji , Tokyo , Japan.
Autophagy
|September 22, 2017
Summary
Legionella pneumophila infection degrades STX17, blocking autophagy and apoptosis. This bacterial serine protease targets the mitochondria-associated ER membrane (MAM), aiding pathogen survival and proliferation.
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Pathogens like Legionella pneumophila evade host defenses, including autophagy and apoptosis, for survival.
- Legionella manipulates host cell vacuoles into ER-like compartments for replication.
- Host-pathogen interactions involve subversion of critical cellular processes.
Purpose of the Study:
- To investigate the role of Legionella effector Lpg1137 in host cell manipulation.
- To determine the mechanism by which Lpg1137 affects autophagy and apoptosis pathways.
- To identify the molecular targets of Lpg1137 within host cells.
Main Methods:
- Protease activity assays to characterize Lpg1137.
- Immunofluorescence and Western blotting to detect STX17 localization and degradation.
- Cellular assays to assess autophagy flux and BAX-induced apoptosis.
Main Results:
- Lpg1137, a serine protease, targets the mitochondria-associated ER membrane (MAM).
- Lpg1137 degrades STX17 (syntaxin 17), a key protein in autophagy and mitochondrial dynamics.
- STX17 degradation by Lpg1137 inhibits both autophagy and BAX-induced apoptosis.
Conclusions:
- Legionella pneumophila utilizes effector Lpg1137 to degrade STX17, thereby blocking host autophagy and apoptosis.
- This mechanism allows the pathogen to evade immune responses and promote intracellular replication.
- Targeting MAM and STX17 represents a novel strategy employed by Legionella to subvert host defenses.
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