Conversion of PtdIns(4,5)P2 into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology
Conversion of PtdIns(4,5)P2 into PtdIns(5)P by the S.flexneri effector IpgD reorganizes host cell morphology
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DOI：
10.1093/emboj/cdf522
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发表时间：
2002-10-01
期刊：
影响因子：
11.4
通讯作者：
Payrastre, B
中科院分区：
文献类型：
--
作者：
Niebuhr, K;Giuriato, S;Payrastre, B
磷酸肌醇在控制包括肌动蛋白细胞骨架组织在内的几种细胞事件中起核心作用。在这里，我们表明，革兰氏阴性病原体福氏志贺菌感染上皮细胞后，毒力因子IpgD直接易位到真核细胞中，并作为一个有效的肌醇4-磷酸酶，特异性地脱磷酸化磷脂酰肌醇4，5-二磷酸[PtdIns（4，5）P-2]成磷脂酰肌醇5-单磷酸[PtdIns（5）P]，然后积累。转染实验表明，PtdIns（4，5）P-2通过IpgD转化为PtdIns（5）P负责宿主细胞的显著形态变化，导致与膜起泡和肌动蛋白丝重塑相关的膜束缚力降低。这些数据提供了一种新的机制，致病性细菌，以促进膜皱褶在进入网站的分子基础。
Phosphoinositides play a central role in the control of several cellular events including actin cytoskeleton organization. Here we show that, upon infection of epithelial cells with the Gram-negative pathogen Shigella flexneri, the virulence factor IpgD is translocated directly into eukaryotic cells and acts as a potent inositol 4-phosphatase that specifically dephosphorylates phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P-2] into phosphatidylinositol 5-monophosphate [PtdIns(5)P] that then accumulates. Transfection experiments indicate that the transformation of PtdIns(4,5)P-2 into PtdIns(5)P by IpgD is responsible for dramatic morphological changes of the host cell, leading to a decrease in membrane tether force associated with membrane blebbing and actin filament remodelling. These data provide the molecular basis for a new mechanism employed by a pathogenic bacterium to promote membrane ruffling at the entry site.