Legionella blocks autophagy by cleaving STX17 (syntaxin 17).
Kohei ArasakiMitsuo TagayaPublished in: Autophagy (2017)
Pathogens subvert host defense systems including autophagy and apoptosis for their survival and proliferation. Legionella pneumophila is a Gram-negative bacterium that grows in alveolar macrophages and causes severe pneumonia. Early during infection Legionella secretes effector proteins that convert the plasma membrane-derived vacuole containing Legionella into an endoplasmic reticulum (ER)-like replicative vacuole. These vacuoles ultimately fuse with the ER, where the pathogen replicates. Recently, we showed that one of the effectors, Lpg1137, is a serine protease that targets the mitochondria-associated ER membrane (MAM) and degrades STX17 (syntaxin 17), a SNARE implicated in macroautophagy/autophagy as well as mitochondria dynamics and membrane trafficking in fed cells. Degradation of STX17 blocks autophagy and BAX-induced apoptosis.
Keyphrases
- induced apoptosis
- endoplasmic reticulum stress
- endoplasmic reticulum
- signaling pathway
- gram negative
- oxidative stress
- cell death
- multidrug resistant
- cell cycle arrest
- pi k akt
- type iii
- estrogen receptor
- early onset
- intensive care unit
- dendritic cells
- breast cancer cells
- antimicrobial resistance
- mechanical ventilation
- community acquired pneumonia