Legionella pneumophila targets autophagosomes and promotes host autophagy during late infection
biorxiv(2021)
摘要
Autophagy is a fundamental eukaryotic process that mediates clearance of unwanted molecules and facilitates nutrient release. The bacterial pathogen Legionella pneumophila establishes an intracellular niche within phagocytes by manipulating host cellular processes, such as autophagy. Effector proteins translocated by L. pneumophila ’s Dot/Icm type IV secretion system have been shown to suppress autophagy. However evidence suggests that overall inhibition of autophagy may be detrimental to the bacterium. As autophagy contributes to cellular homeostasis and nutrient acquisition, L. pneumophila may translocate effectors that promote autophagy for these benefits. Here, we show that effector protein Lpg2411 binds phosphatidylinositol-3-phosphate lipids and preferentially binds autophagosomes. Translocated Lpg2411 accumulates late during infection and co-localizes with the autophagy receptor p62 and ubiquitin. Furthermore, autophagy is inhibited to a greater extent in host cells infected with a mutant strain lacking Lpg2411 compared to those infected with wild-type L. pneumophila, indicating that Lpg2411 stimulates autophagy to support the bacterium’s intracellular lifestyle.
Summary Legionella pneumophila translocates several effector proteins that inhibit autophagic processes. In this study, we find that the effector protein Lpg2411 targets autophagosomes during late stages of infection and promotes autophagy.
* HA
: hemagglutinin
CFU
: colony-forming units
CHO
: Chinese hamster ovary cells
LCV
: Legionella -containing vacuole
MOC
: Mander’s Overlap Coefficient
MOI
: Multiplicity of infection
PIP
: phosphatidylinositol phosphate
PI(3)P
: phosphatidylinositol-3-phosphate
PI(4)P
: phosphatidylinositol-4-phosphate
T4SS
: type IV secretion system
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关键词
host autophagy,autophagosomes,late infection
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