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Rho 依赖性膜折叠导致志贺氏菌进入上皮细胞。

Rho-dependent membrane folding causes Shigella entry into epithelial cells.

作者信息

Adam T, Giry M, Boquet P, Sansonetti P

机构信息

Unité de Pathogénie Microbienne Moléculaire, INSERM U389, Paris, France.

出版信息

EMBO J. 1996 Jul 1;15(13):3315-21.

PMID:8670832
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC451894/
Abstract

The small GTPase rho is functionally involved in the formation of cytoskeletal structures like stress fibers or focal adhesion plaques. Shigella entry into HeLa cells induces a blossom-like membrane structure at the bacterial entry site. We show here that this membrane-folding process is rho-dependent. The three rho isoforms were recruited into bacterial entry sites with differential localization relative to the membrane structure. A rho-specific inhibitor abolished Shigella-induced membrane folding and impaired bacterial entry accordingly. S1-myosin labeling indicated that rho was involved in Shigella-induced actin polymerization but not actin nucleation in the bacterial invasion site. This provides a major link in the signalization cascade allowing entry of a bacterial pathogen into a eukaryotic cell.

摘要

小GTP酶rho在功能上参与细胞骨架结构的形成,如应力纤维或粘着斑。志贺氏菌进入HeLa细胞会在细菌进入位点诱导出一种花状膜结构。我们在此表明,这种膜折叠过程依赖于rho。三种rho亚型被招募到细菌进入位点,相对于膜结构具有不同的定位。一种rho特异性抑制剂消除了志贺氏菌诱导的膜折叠,并相应地损害了细菌的进入。S1-肌球蛋白标记表明rho参与了志贺氏菌诱导的细菌入侵位点的肌动蛋白聚合,但不参与肌动蛋白成核。这在信号级联反应中提供了一个主要环节,使细菌病原体能够进入真核细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/898443e43538/emboj00013-0113-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/a1b377421ab6/emboj00013-0110-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/77260e5517e0/emboj00013-0110-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/1a5ce19e5cdc/emboj00013-0111-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/d9c590d0e25f/emboj00013-0112-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/898443e43538/emboj00013-0113-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/a1b377421ab6/emboj00013-0110-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/77260e5517e0/emboj00013-0110-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/1a5ce19e5cdc/emboj00013-0111-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/d9c590d0e25f/emboj00013-0112-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/222b/451894/898443e43538/emboj00013-0113-a.jpg

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本文引用的文献

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A chimeric toxin to study the role of the 21 kDa GTP binding protein rho in the control of actin microfilament assembly.一种用于研究21 kDa GTP结合蛋白rho在肌动蛋白微丝组装调控中作用的嵌合毒素。
EMBO J. 1993 Mar;12(3):921-31. doi: 10.1002/j.1460-2075.1993.tb05733.x.
2
Involvement of Rho p21 small GTP-binding protein and its regulator in the HGF-induced cell motility.Rho p21小GTP结合蛋白及其调节因子参与肝细胞生长因子诱导的细胞运动。
Oncogene. 1994 Jan;9(1):273-9.
3
Identification of two human Rho GDP dissociation inhibitor proteins whose overexpression leads to disruption of the actin cytoskeleton.
该研究揭示了一种钙/钙蛋白酶依赖的机制,用于抑制 SUMO 化。
Elife. 2017 Dec 12;6:e27444. doi: 10.7554/eLife.27444.
4
Sphingosine 1-Phosphate Activation of EGFR As a Novel Target for Meningitic Escherichia coli Penetration of the Blood-Brain Barrier.1-磷酸鞘氨醇激活表皮生长因子受体作为脑膜炎性大肠杆菌穿越血脑屏障的新靶点
PLoS Pathog. 2016 Oct 6;12(10):e1005926. doi: 10.1371/journal.ppat.1005926. eCollection 2016 Oct.
5
Macropinosomes are Key Players in Early Shigella Invasion and Vacuolar Escape in Epithelial Cells.巨吞饮小泡是志贺氏菌早期侵入上皮细胞及从液泡逃逸过程中的关键参与者。
PLoS Pathog. 2016 May 16;12(5):e1005602. doi: 10.1371/journal.ppat.1005602. eCollection 2016 May.
6
Enzymatically active Rho and Rac small-GTPases are involved in the establishment of the vacuolar membrane after Toxoplasma gondii invasion of host cells.在刚地弓形虫入侵宿主细胞后,具有酶活性的 Rho 和 Rac 小分子 GTP 酶参与液泡膜的建立。
BMC Microbiol. 2013 May 30;13:125. doi: 10.1186/1471-2180-13-125.
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The origins of phagocytosis and eukaryogenesis.吞噬作用与真核生物起源
Biol Direct. 2009 Feb 26;4:9. doi: 10.1186/1745-6150-4-9.
8
GEF-H1 mediated control of NOD1 dependent NF-kappaB activation by Shigella effectors.GEF-H1介导志贺氏菌效应蛋白对NOD1依赖性NF-κB激活的调控。
PLoS Pathog. 2008 Nov;4(11):e1000228. doi: 10.1371/journal.ppat.1000228. Epub 2008 Nov 28.
9
The C-terminus of IpaC is required for effector activities related to Shigella invasion of host cells.IpaC的C末端是志贺氏菌侵袭宿主细胞相关效应子活性所必需的。
Microb Pathog. 2008 Oct;45(4):282-9. doi: 10.1016/j.micpath.2008.06.003. Epub 2008 Jul 4.
10
Saccharomyces boulardii interferes with Shigella pathogenesis by postinvasion signaling events.布拉酵母菌通过侵袭后信号事件干扰志贺菌发病机制。
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两种人类Rho GDP解离抑制蛋白的鉴定,其过表达会导致肌动蛋白细胞骨架的破坏。
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Salmonella typhimurium induces membrane ruffling by a growth factor-receptor-independent mechanism.鼠伤寒沙门氏菌通过一种不依赖生长因子受体的机制诱导膜皱褶形成。
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5
ADP-ribosylation of rho p21 inhibits lysophosphatidic acid-induced protein tyrosine phosphorylation and phosphatidylinositol 3-kinase activation in cultured Swiss 3T3 cells.rho p21的ADP核糖基化抑制培养的瑞士3T3细胞中溶血磷脂酸诱导的蛋白酪氨酸磷酸化和磷脂酰肌醇3激酶激活。
J Biol Chem. 1993 Nov 25;268(33):24535-8.
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Activation of platelet phosphatidylinositide 3-kinase requires the small GTP-binding protein Rho.血小板磷脂酰肌醇3激酶的激活需要小GTP结合蛋白Rho。
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J Biol Chem. 1994 Apr 8;269(14):10706-12.
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rac p21 is involved in insulin-induced membrane ruffling and rho p21 is involved in hepatocyte growth factor- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced membrane ruffling in KB cells.Rac p21参与胰岛素诱导的膜皱襞形成,而Rho p21参与肝细胞生长因子和12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)诱导的KB细胞的膜皱襞形成。
Mol Cell Biol. 1994 Apr;14(4):2447-56. doi: 10.1128/mcb.14.4.2447-2456.1994.
9
The GDP-bound form of the small G protein Rac1 p21 is a potent activator of the superoxide-forming NADPH oxidase of macrophages.小G蛋白Rac1 p21的GDP结合形式是巨噬细胞中超氧化物形成的NADPH氧化酶的有效激活剂。
J Biol Chem. 1994 Mar 11;269(10):7055-8.
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Small GTP-binding proteins and the regulation of the actin cytoskeleton.小GTP结合蛋白与肌动蛋白细胞骨架的调控
Annu Rev Cell Biol. 1994;10:31-54. doi: 10.1146/annurev.cb.10.110194.000335.