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.

在感染过程中，细胞内细菌病原体将多种效应子转移到宿主细胞中，从而改变宿主膜的运输以使其受益。我们发现了一个由细菌磷酸肌醇激酶及其相反的磷酸酶组成的自组织系统，该系统形成时空模式（包括行波）以重塑宿主细胞膜。军团菌效应子 MavQ 是一种磷脂酰肌醇 (PI) 3-激酶，靶向内质网 (ER)。即使在没有其他细菌成分的情况下，MavQ 和军团菌PI 3-磷酸酶 SidP 也会驱动 ER 上的 PI 3-磷酸快速周转，并自发形成沿 ER 子域传播的行波，诱导囊泡和小管出芽。因此，细菌可以利用自组织膜靶向机制来劫持宿主细胞结构以求生存。