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首页> 外文期刊>Cell motility and the cytoskeleton >Inhibition of cytokinesis by Clostridium difficile toxin B and cytotoxic necrotizing factors--reinforcing the critical role of RhoA in cytokinesis.
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Inhibition of cytokinesis by Clostridium difficile toxin B and cytotoxic necrotizing factors--reinforcing the critical role of RhoA in cytokinesis.

机译：艰难梭菌毒素B和细胞毒性坏死因子对细胞分裂的抑制作用-增强了RhoA在细胞分裂中的关键作用。

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摘要

Low molecular weight GTP-binding proteins of the Rho family control the organization of the actin cytoskeleton in eukaryotic cells. RhoA governs the formation of actin stress fibers and is responsible for the formation of the contractile ring in cytokinesis. Cytokinesis completion requires RhoA inactivation resulting in disassembly of the contractile ring. Cytokinesis thus requires switching of RhoA activity. This switch of RhoA activity is blocked by Rho-modifying bacterial protein toxins that either activate or inactivate RhoA by covalent modifications. Exoenzyme C3 from Clostridium limosum (C3-lim) and Clostridium difficile toxin B (TcdB) inactivate RhoA by mono-ADP-ribosylation and mono-glucosylation, respectively. Cytotoxic necrotizing factors (CNF), produced by either Yersinia pseudotuberculosis (CNFY) or uropathogenic strains of E. coli (CNF1), deamidate and thereby activate RhoA. This study provides evidence that RhoA-activating as well as RhoA-inactivating toxins cause inhibition of cytokinesis and cell division. The toxins' effects on cytokinesis were analyzed in Hela cells synchronized using the thymidine double block technique. Treatment of G2-phase cells with either the RhoA-activating CNFY or CNF1 or the RhoA-inactivating C3-lim or TcdB resulted in cytokinesis inhibition, as evidenced by the formation of a 4N population on flow cytometry, the inhibition of contractile ring formation, and the formation of bi-nucleated cells. While TcdB and CNF1 modify a broad-spectrum of Rho proteins, C3-lim and CNFY specifically target RhoA. Since C3-lim and CNFY both caused cytokinesis inhibition, our study re-inforces the critical role of RhoA (not Rac1 or Cdc42) in cytokinesis and cell division.
机译：Rho家族的低分子量GTP结合蛋白控制真核细胞中肌动蛋白细胞骨架的组织。 RhoA控制肌动蛋白应激纤维的形成，并负责细胞分裂的收缩环的形成。细胞分裂完成需要RhoA失活，导致收缩环的拆卸。因此，细胞分裂需要切换RhoA活性。 RhoA活性的这种转换被Rho修饰的细菌蛋白毒素阻断，该毒素通过共价修饰激活或灭活RhoA。柠檬酸梭菌（C3-lim）和艰难梭菌毒素B（TcdB）的外切酶C3分别通过单ADP-核糖基化和单糖基化使RhoA失活。由耶尔森氏菌假结核耶尔森氏菌（CNFY）或大肠杆菌的尿毒症毒株（CNF1）产生的细胞毒性坏死因子（CNF）会脱氨基，从而激活RhoA。这项研究提供了证据，即RhoA激活和RhoA灭活毒素引起细胞分裂和细胞分裂的抑制。使用胸苷双阻断技术同步分析了Hela细胞中毒素对胞质分裂的影响。用激活RhoA的CNFY或CNF1或激活RhoA的C3-lim或TcdB处理G2期细胞可导致胞质分裂抑制，如流式细胞术中形成4N群体，抑制收缩环形成，并形成双核细胞。尽管TcdB和CNF1修饰了广谱的Rho蛋白，但C3-lim和CNFY特异性靶向RhoA。由于C3-lim和CNFY均引起胞质分裂抑制，因此我们的研究加强了RhoA（不是Rac1或Cdc42）在胞质分裂和细胞分裂中的关键作用。

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