The stress protectant trehalose is synthesized in Acinetobacter baumannii from UPD-glucose and glucose-6-phosphase via the OtsA/OtsB pathway. Previous studies proved that deletion of otsB led to a decreased virulence, the inability to grow at 45°C and a slight reduction of growth at high salinities indicating that trehalose is the cause of these phenotypes. We have questioned this conclusion by producing ∆otsA and ∆otsBA mutants and studying their phenotypes. Only deletion of otsB, but not deletion of otsA or otsBA, led to growth impairments at high salt and high temperature. The intracellular concentrations of trehalose and trehalose-6-phosphate were measured by NMR or enzymatic assay. Interestingly, none of the mutants accumulated trehalose any more but the ∆otsB mutant with its defect in trehalose-6-phosphate phosphatase activity accumulated trehalose-6-phosphate. Moreover, expression of otsA in a ∆otsB background under conditions where trehalose synthesis is not induced led to growth inhibition and the accumulation of trehalose-6-phosphate. Our results demonstrate that trehalose-6-phosphate affects multiple physiological activities in A. baumannii ATCC 19606.

译文

压力保护剂海藻糖由UPD-葡萄糖和glucose-6-phosphase通过OtsA/OtsB途径在鲍曼不动杆菌中合成。先前的研究证明,otsB的缺失导致毒力降低,在45 °C下无法生长以及在高盐度下的生长略有降低,这表明海藻糖是这些表型的原因。我们通过产生 ∆ otsa和 ∆ otsba突变体并研究其表型来质疑这一结论。仅删除otsB,而不删除otsA或otsBA,在高盐和高温下导致生长受损。通过NMR或酶法测定海藻糖和trehalose-6-phosphate的细胞内浓度。有趣的是,除了trehalose-6-phosphate磷酸酶活性缺陷的 ∆ otsb突变体外,没有一个突变体再积累海藻糖trehalose-6-phosphate。此外,在不诱导海藻糖合成的条件下,otsA在 ∆ otsb背景中的表达导致生长抑制和trehalose-6-phosphate积累。我们的结果表明,trehalose-6-phosphate影响鲍曼不动杆菌ATCC 19606的多种生理活动。

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