TY - JOUR
T1 - Dynamic remodeling of host membranes by self-organizing bacterial effectors
AU - Hsieh, Ting Sung
AU - Lopez, Victor A.
AU - Black, Miles H.
AU - Osinski, Adam
AU - Pawłowski, Krzysztof
AU - Tomchick, Diana R.
AU - Liou, Jen
AU - Tagliabracci, Vincent S.
N1 - Publisher Copyright:
Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
PY - 2021/5/28
Y1 - 2021/5/28
N2 - 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 membranetargeting mechanism to hijack host cellular structures for survival.
AB - 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 membranetargeting mechanism to hijack host cellular structures for survival.
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U2 - 10.1126/science.aay8118
DO - 10.1126/science.aay8118
M3 - Review article
C2 - 33927055
AN - SCOPUS:85106733735
SN - 0036-8075
VL - 372
JO - Science
JF - Science
IS - 6545
ER -