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Global Transcriptional Analysis of Dehydrated Salmonella enterica Serovar Typhimurium

机译:脱水沙门氏菌血清型鼠伤寒沙门氏菌的全球转录分析。

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Despite the scientific and industrial importance of desiccation tolerance in Salmonella , knowledge regarding its genetic basis is still scarce. In the present study, we performed a transcriptomic analysis of dehydrated and water-suspended Salmonella enterica serovar Typhimurium using microarrays. Dehydration induced expression of 90 genes and downregulated that of 7 genes. Ribosomal structural genes represented the most abundant functional group with a relatively higher transcription during dehydration. Other main induced functional groups included genes involved in amino acid metabolism, energy production, ion transport, transcription, and stress response. The highest induction was observed in the kdpFABC operon, encoding a potassium transport channel. Knockout mutations were generated in nine upregulated genes. Five mutants displayed lower tolerance to desiccation, implying the involvement of the corresponding genes in the adaptation of Salmonella to desiccation. These included genes encoding the isocitrate-lyase AceA, the lipid A biosynthesis palmitoleoyl-acyltransferase Ddg, the modular iron-sulfur cluster scaffolding protein NifU, the global regulator Fnr, and the alternative sigma factor RpoE. Notably, these proteins were previously implicated in the response of Salmonella to oxidative stress, heat shock, and cold shock. A strain with a mutation in the structural gene kdpA had a tolerance to dehydration comparable to that of the parent strain, implying that potassium transport through this system is dispensable for early adaptation to the dry environment. Nevertheless, this mutant was significantly impaired in long-term persistence during cold storage. Our findings indicate the involvement of a relatively small fraction of the Salmonella genome in transcriptional adjustment from water to dehydration, with a high prevalence of genes belonging to the protein biosynthesis machinery.
机译:尽管沙门氏菌的耐干燥性在科学和工业上很重要,但有关其遗传基础的知识仍很匮乏。在本研究中,我们使用微阵列芯片对脱水和水悬浮肠沙门氏菌血清鼠伤寒沙门氏菌进行了转录组学分析。脱水诱导90个基因的表达,并下调7个基因的表达。核糖体结构基因代表最丰富的官能团,在脱水过程中具有相对较高的转录。其他主要的诱导功能基团包括涉及氨基酸代谢,能量产生,离子转运,转录和应激反应的基因。在kdpFABC操纵子中观察到最高诱导,编码钾转运通道。在9个上调的基因中产生了敲除突变。五个突变体表现出较低的干燥耐受性,这意味着相应的基因参与了沙门氏菌对干燥的适应。这些基因包括编码异柠檬酸裂合酶AceA,脂质A生物合成棕榈油酰基-酰基转移酶Ddg,模块化铁硫簇支架蛋白NifU,全局调节因子Fnr和替代的sigma因子RpoE的基因。值得注意的是,这些蛋白质以前与沙门氏菌对氧化应激,热休克和冷休克的反应有关。结构基因kdpA突变的菌株对脱水的耐受性与亲代菌株相当,这意味着钾通过该系统的运输对于早期适应干燥环境是必不可少的。然而,该突变体在冷藏期间的长期持久性显着受损。我们的研究结果表明,沙门氏菌基因组中相对较小的部分参与了从水到脱水的转录调节,并且属于蛋白质生物合成机制的基因普遍存在。

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