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DNA 超螺旋结构受到环境因素和 FIS 在大肠杆菌和沙门氏菌中的差异调节。

DNA supercoiling is differentially regulated by environmental factors and FIS in Escherichia coli and Salmonella enterica.

机构信息

Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin 2, Ireland.

出版信息

Mol Microbiol. 2011 Apr;80(1):85-101. doi: 10.1111/j.1365-2958.2011.07560.x. Epub 2011 Feb 15.

DOI:10.1111/j.1365-2958.2011.07560.x
PMID:21276095
Abstract

Although Escherichia coli and Salmonella enterica inhabit similar niches and employ similar genetic regulatory programmes, we find that they differ significantly in their DNA supercoiling responses to environmental and antibiotic challenges. Whereas E. coli demonstrates large dynamic transitions in supercoiling in response to growth phase, osmotic pressure and novobiocin treatment, supercoiling levels are much less variable in S. enterica. The FIS protein is a global regulator of supercoiling in E. coli, but it was found to have less influence over supercoiling control in S. enterica. These inter-species differences fine-tune gene promoters to endogenous supercoiling and FIS levels. Transferring a Salmonella virulence gene promoter (P(ssrA) ) into a new enteric host (E. coli) caused aberrant expression in response to stimulatory signals. Reciprocal horizontal transfer of topA promoters, which control expression of topoisomerase I, between E. coli and S. enterica revealed how these orthologous promoters have evolved to respond differentially to FIS and supercoiling levels in their cognate species. This also identified a previously unrecognized osmoregulation of topA expression that is independent of FIS and supercoiling in both E. coli and S. enterica. These findings suggest that E. coli and S. enterica may be unexpectedly divergent in their global regulation of cellular physiology.

摘要

尽管大肠杆菌和肠炎沙门氏菌栖息在相似的生态位,并采用类似的遗传调控程序,但我们发现它们在对外界环境和抗生素的挑战时,其 DNA 超螺旋的反应存在显著差异。虽然大肠杆菌在生长阶段、渗透压和新生霉素处理时会表现出超螺旋的大幅动态变化,但肠炎沙门氏菌的超螺旋水平变化要小得多。FIS 蛋白是大肠杆菌中超螺旋的全局调控因子,但它对肠炎沙门氏菌中超螺旋控制的影响较小。这些种间差异使基因启动子精细地适应内源性超螺旋和 FIS 水平。将沙门氏菌毒力基因启动子(P(ssrA))转入新的肠宿主(大肠杆菌)会导致其对刺激信号的异常表达。拓扑异构酶 I 的 topA 启动子在大肠杆菌和肠炎沙门氏菌之间的相互水平转移,揭示了这些同源启动子如何在其同源物种中进化,以对 FIS 和超螺旋水平产生不同的反应。这也确定了一个以前未被识别的渗透压对 topA 表达的调节,这在大肠杆菌和肠炎沙门氏菌中都是独立于 FIS 和超螺旋的。这些发现表明,大肠杆菌和肠炎沙门氏菌在其细胞生理学的全局调控方面可能出乎意料地存在分歧。

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