Institute of Toxicology, Hannover Medical School, D-30625 Hannover, Germany.
Int J Biochem Cell Biol. 2013 Aug;45(8):1767-75. doi: 10.1016/j.biocel.2013.05.020. Epub 2013 May 31.
RhoB is the only member of the Rho subfamily of small GTPases, which is classified as an immediate early gene product. RhoB is up-regulated in response to growth factors as well as cytotoxic and genotoxic agents. Clostridial glucosylating toxins have been reported to evoke pronounced RhoB expression, based on the inactivation of Rho/Ras proteins. In this study, we report on a long lasting expression of RhoB in cultured cells upon activation of Rho proteins by the cytotoxic necrotizing factor 1 (CNF1) from Escherichia coli. The observations of this study highlight a new pathway involving Rac1, which positively regulates the activity of the rhoB promoter and RhoB expression. Conversely, the isomeric cytotoxic necrotizing factor from Yersinia pseudotuberculosis (CNFy) drives GTP-loading of basal RhoB but fails to cause activation of the rhoB promoter and thus its expression. CNF1 inhibits cytokinesis and induces the formation of bi-nucleated (tetraploid) cells. Upon long term treatment with CNF1, RhoB(-/-) mouse embryonic fibroblasts (MEFs) exhibit DNA fragmentation, phosphatidylserine exposure, and loss of membrane integrity, while RhoB(+/-) MEFs persist as bi-nucleated (tetraploid) cells without any signs of cell death. In conclusion, the cytoprotective RhoB response is not only evoked by bacterial protein toxins inactivating Rho/Ras proteins but also by the Rac1-activating toxin CNF1.
RhoB 是 Rho 亚家族小分子 GTP 酶的唯一成员,被归类为即时早期基因产物。RhoB 受生长因子以及细胞毒性和遗传毒性试剂的刺激而上调。基于 Rho/Ras 蛋白的失活,已报道梭菌糖基化毒素可引起 RhoB 的明显表达。在这项研究中,我们报告了在培养细胞中 Rho 蛋白被细胞毒性坏死因子 1(CNF1)激活后,RhoB 的持续表达。本研究的观察结果突出了一条新的途径,涉及 Rac1,它正向调节 rhoB 启动子的活性和 RhoB 的表达。相反,来自假结核耶尔森氏菌的同型细胞毒性坏死因子(CNFy)驱动基础 RhoB 的 GTP 加载,但不能激活 rhoB 启动子,因此不能表达其表达。CNF1 抑制细胞分裂并诱导形成双核(四倍体)细胞。在用 CNF1 长期处理后,RhoB(-/-) 小鼠胚胎成纤维细胞(MEF)表现出 DNA 片段化、磷脂酰丝氨酸暴露和膜完整性丧失,而 RhoB(+/-) MEF 则保持为双核(四倍体)细胞,没有任何细胞死亡的迹象。总之,细胞保护的 RhoB 反应不仅由失活 Rho/Ras 蛋白的细菌蛋白毒素引起,也由激活 Rac1 的毒素 CNF1 引起。