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首页> 外文期刊>Infection and immunity >Escherichia coli cytolethal distending toxin blocks the HeLa cell cycle at the G2/M transition by preventing cdc2 protein kinase dephosphorylation and activation.
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Escherichia coli cytolethal distending toxin blocks the HeLa cell cycle at the G2/M transition by preventing cdc2 protein kinase dephosphorylation and activation.

机译：大肠杆菌细胞致死性扩张毒素通过阻止cdc2蛋白激酶去磷酸化和激活来阻止HeLa细胞在G2 / M转变时的细胞周期。

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摘要

Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized HeLa cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes cell accumulation in G2 and not in M, that it does not slow the progression of cells through S phase, and that it does not affect the normal increase of cyclin B1 from late S to G2. On the other hand, we show that CDT inhibits the kinase activity of cdc2 by preventing its dephosphorylation, an event which, in normal cells, triggers mitosis. This inhibitory activity was demonstrated for the three partially related CDTs so far described for E. coli. Moreover, we provide evidence that cells exposed to CDT during G2 and M phases are blocked only at the subsequent G2 phase. This observation means that the toxin triggers a mechanism of cell arrest that is initiated in S phase and therefore possibly related to the DNA damage checkpoint system.
机译：细胞致死性扩张性毒素（CDT）构成了一种新兴的异质细菌毒素家族，其共同的生物学特性是通过阻止细胞在G2 / M期的周期来抑制培养细胞的增殖。在这项研究中，我们调查了同步HeLa细胞培养中大肠杆菌CDT引起的阻断的分子机制。为此，我们专门研究了决定进入有丝分裂的复合物的两个亚基的行为，即调节蛋白cyclin B1和催化单元cdc2蛋白激酶。因此，我们证明CDT会导致细胞在G2中而不是在M中蓄积，它不会减慢细胞通过S期的进程，也不会影响细胞周期蛋白B1从S晚期到G2的正常增加。另一方面，我们显示CDT通过阻止cdc2的去磷酸化来抑制cdc2的激酶活性，该事件在正常细胞中触发有丝分裂。迄今为止对大肠杆菌所描述的三种部分相关的CDT均显示出这种抑制活性。此外，我们提供的证据表明，在G2和M期中暴露于CDT的细胞仅在随后的G2期被阻断。该观察结果表明该毒素触发了细胞停滞机制，该机制在S期开始，因此可能与DNA损伤检查点系统有关。

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