期刊
SCIENCE
卷 372, 期 6545, 页码 935-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aay8118
关键词
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During infection, bacterial pathogens can manipulate host cellular membranes by utilizing a self-organizing system involving bacterial kinases and phosphatases, such as the Legionella effector MavQ. This mechanism allows bacteria to hijack host cellular structures for survival by driving rapid turnover of phosphoinositides and inducing vesicle and tubule budding.
During infection, intracellular bacterial pathogens translocate a variety of effectors into host cells that modify host membrane trafficking for their benefit. We found a self-organizing system consisting of a bacterial phosphoinositide kinase and its opposing phosphatase that formed spatiotemporal patterns, including traveling waves, to remodel host cellular membranes. The Legionella effector MavQ, a phosphatidylinositol (PI) 3-kinase, was targeted to the endoplasmic reticulum (ER). MavQ and the Legionella PI 3-phosphatase SidP, even in the absence of other bacterial components, drove rapid PI 3-phosphate turnover on the ER and spontaneously formed traveling waves that spread along ER subdomains inducing vesicle and tubule budding. Thus, bacteria can exploit a self-organizing membrane-targeting mechanism to hijack host cellular structures for survival.
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