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.

中文翻译：

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海藻6-磷酸介导的鲍曼不动杆菌的表型改变。

应力保护剂海藻糖是通过UtsA / OtsB途径由UPD-葡萄糖和葡萄糖-6-磷酸酶在鲍曼不动杆菌中合成的。以前的研究证明，删除otsB会导致毒力降低，无法在45°C下生长以及在高盐度下生长略有减少，这表明海藻糖是这些表型的原因。我们通过生产Δ质疑这个结论奖励计划和Δ otsBA突变和研究他们的表型。只有删除otsB，但不删除的奖励计划或otsBA，导致在高盐和高温下生长受到损害。通过NMR或酶法测定细胞内海藻糖和海藻糖-6-磷酸的浓度。有趣的是，除了ΔotsB突变体（其海藻糖-6-磷酸磷酸酶活性存在缺陷）以外，没有其他突变体累积海藻糖-6-磷酸。此外，表达奖励计划在一个Δ otsB条件下背景其中海藻糖合成不诱发导致生长抑制和海藻糖-6-磷酸的积累。我们的结果表明，6-海藻糖会影响鲍曼不动杆菌ATCC 19606中的多种生理活性。