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首页> 外文期刊>Cytoskeleton >Contractile Actin Cables Induced by Bacillus anthracis Lethal Toxin Depend on the Histone Acetylation Machinery
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Contractile Actin Cables Induced by Bacillus anthracis Lethal Toxin Depend on the Histone Acetylation Machinery

机译：炭疽芽孢杆菌致死毒素诱导的收缩性肌动蛋白电缆取决于组蛋白乙酰化机制

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It remains a challenge to decode the molecular basis of the long-term actin cytoskeleton rearrangements that are governed by the reprogramming of gene expression. Bacillus anthracis lethal toxin (LT) inhibits mitogen-activated protein kinase (MAPK) signaling, thereby modulating gene expression, with major consequences for actin cytoskeleton organization and the loss of endothelial barrier function. Using a laser ablation approach, we characterized the contractile and tensile mechanical properties of LT-induced stress fibers. These actin cables resist pulling forces that are transmitted at cell-matrix interfaces and at cell-cell discontinuous adherens junctions. We report that treating the cells with trichostatin A (TSA), a broad range inhibitor of histone deacetylases (HDACs), or with MS-275, which targets HDAC1, 2 and 3, induces stress fibers. LT decreased the cellular levels of HDAC1, 2 and 3 and reduced the global HDAC activity in the nucleus. Both the LT and TSA treatments induced Rnd3 expression, which is required for the LT-mediated induction of actin stress fibers. Furthermore, we reveal that treating the LT-intoxicated cells with garcinol, an inhibitor of histone acetyl-transferases (HATs), disrupts the stress fibers and limits the monolayer barrier dysfunctions. These data demonstrate the importance of modulating the flux of protein acetylation in order to control actin cytoskeleton organization and the endothelial cell monolayer barrier. (C) 2015 Wiley Periodicals, Inc.
机译：解码受基因表达重编程控制的长期肌动蛋白细胞骨架重排的分子基础仍然是一个挑战。炭疽芽孢杆菌致死毒素（LT）抑制有丝分裂原激活的蛋白激酶（MAPK）信号传导，从而调节基因表达，对肌动蛋白细胞骨架的组织和内皮屏障功能的丧失产生重大影响。使用激光烧蚀方法，我们表征了LT诱导的应力纤维的收缩和拉伸机械性能。这些肌动蛋白电缆抵抗在细胞-基质界面和细胞-细胞不连续粘附连接处传递的拉力。我们报告说，用曲古抑菌素A（TSA），组蛋白脱乙酰基酶（HDACs）的广泛抑制剂或以HDAC1、2和3为目标的MS-275处理细胞会诱导应激纤维。 LT降低了HDAC1、2和3的细胞水平，并降低了细胞核中的整体HDAC活性。 LT和TSA处理均诱导Rnd3表达，这是LT介导的肌动蛋白应激纤维诱导所必需的。此外，我们揭示了用garcinol（一种组蛋白乙酰基转移酶（HATs）的抑制剂）处理LT感染的细胞，会破坏应激纤维并限制单层屏障功能障碍。这些数据表明调节蛋白乙酰化通量以控制肌动蛋白细胞骨架组织和内皮细胞单层屏障的重要性。 （C）2015年Wiley Periodicals，Inc.

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