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首页> 外文期刊>Genes & Genetic Systems >Assessment of transcriptional responses of Bacillus subtilis cells to the antibiotic enduracidin, which interferes with cell wall synthesis, using a high-density tiling chip.
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Assessment of transcriptional responses of Bacillus subtilis cells to the antibiotic enduracidin, which interferes with cell wall synthesis, using a high-density tiling chip.

机译：使用高密度贴图芯片评估枯草芽孢杆菌细胞对抗生素抗坏血酸的转录反应，这会干扰细胞壁的合成。

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摘要

The cell envelope is the target for many antibiotics. In Gram-positive bacteria, membrane alterations and dysfunction caused by antibiotics are sensed mainly by two classes of signal transduction systems: the ECF sigma factors and the two-component signal transduction systems (TCSs). Enduracidin is an antibiotic that inhibits the transglycosylation step of peptidoglycan biosynthesis, and is an attractive target for further antibiotic development studies. We assessed transcriptional responses to enduracidin in Bacillus subtilis cells using a high-density tiling chip, and compared the results with responses to bacitracin, which inhibits the lipid II cycle of peptidoglycan synthesis. We exploited the quantitative advantage of the tiling chip to introduce a new criterion, an increase in transcriptional level, in addition to the conventional induction ratio, in order to distinguish genes of biological significance from those with lower induction ratios. Our results indicate that introduction of the new criterion led to unambiguous identification of core transcriptional responses to antibiotics, with a reduction in the number of possible background genes, compared to previous results obtained using gene arrays. We identified 129 genes that were significantly upregulated by enduracidin and/or bacitracin. Notably, we found that inactivation of the LiaRS TCS, which was the system most strongly induced by the two antibiotics, resulted in increased sensitivity to enduracidin, probably through a failure to induce LiaIH proteins. We noted that 33 genes belonging to the SigM regulon were induced by both antibiotics. Consistent with stronger induction of the SigM regulon in enduracidin-treated cells, inactivation of sigM resulted in increased sensitivity to enduracidin. In addition, and for the first time, we found that the Spx regulon was induced in cells challenged by enduracidin and bacitracin, suggesting that thiol-oxidative stress occurred in cells treated with antibiotics. These findings contribute to further our understanding of the molecular nature of genetic systems involved in antibiotic resistance.
机译：细胞包膜是许多抗生素的靶标。在革兰氏阳性细菌中，抗生素引起的膜改变和功能障碍主要通过两类信号转导系统来感知：ECF sigma因子和两组分信号转导系统（TCSs）。 Enduracidin是一种抑制肽聚糖生物合成的转糖基化步骤的抗生素，并且是进行进一步抗生素开发研究的有吸引力的靶标。我们使用高密度切片芯片评估了枯草芽孢杆菌细胞中耐力酸的转录反应，并将结果与​​杆菌肽的反应进行了比较，杆菌肽抑制了肽聚糖合成的脂质II循环。我们利用平铺芯片的数量优势，引入了一种新的标准，除了常规的诱导率外，还提高了转录水平，从而将具有生物学意义的基因与具有较低诱导率的基因区分开来。我们的结果表明，与使用基因阵列获得的以前的结果相比，新标准的引入导致对抗生素的核心转录反应的明确鉴定，并且可能的背景基因数量减少了。我们鉴定了129个基因，它们被Enduracidin和/或杆菌肽显着上调。值得注意的是，我们发现，由两种抗生素最强烈诱导的系统LiaRS TCS失活，可能是由于未能诱导LiaIH蛋白而导致了对Enduracidin的敏感性增加。我们注意到，两种抗生素均诱导了SigM regulon的33个基因。 sigM 的失活与在经耐多酸治疗的细胞中SigM regulon的更强诱导作用相一致，从而导致对耐多酸的敏感性增加。此外，我们首次发现，在耐力酸和杆菌肽攻击的细胞中诱导了Spx调节子，这表明在用抗生素处理的细胞中发生了巯基氧化应激。这些发现有助于我们进一步了解涉及抗生素抗性的遗传系统的分子性质。

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