An important prelude to bacterial infection is the ability of a pathogen to survive independently of the host and to withstand environmental stress. The compatible solute trehalose has previously been connected with diverse abiotic stress tolerances, particularly osmotic shock. In this study, we combine molecular biology and biochemistry to dissect the trehalose metabolic network in the opportunistic human pathogen Pseudomonas aeruginosa PA01 and define its role in abiotic stress protection. We show that trehalose metabolism in PA01 is integrated with the biosynthesis of branched α-glucan (glycogen), with mutants in either biosynthetic pathway significantly compromised for survival on abiotic surfaces. While both trehalose and α-glucan are important for abiotic stress tolerance, we show they counter distinct stresses. Trehalose is vital to the PA01 osmotic stress response, with trehalose synthesis mutants displaying severely compromised growth in elevated salt conditions. However, trehalose does not contribute directly to the PA01 desiccation response. Rather, desiccation tolerance is mediated directly by GlgE-derived α-glucan, with deletion of the glgE synthase gene compromising PA01 survival in low humidity but having little effect on osmotic sensitivity. Desiccation tolerance is independent of trehalose concentration, marking a clear distinction between the roles of these two molecules in mediating responses to abiotic stress.

中文翻译：

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海藻糖和α-葡聚糖介导铜绿假单胞菌不同的非生物应激反应

细菌感染的重要前奏是病原体独立于宿主生存并承受环境压力的能力。相容的溶质海藻糖以前曾与多种非生物胁迫耐受性有关，尤其是渗透性休克。在这项研究中，我们结合分子生物学和生物化学来剖析机会性人类病原体铜绿假单胞菌PA01中的海藻糖代谢网络，并定义其在非生物胁迫保护中的作用。我们显示，PA01中的海藻糖代谢与分支α-葡聚糖（糖原）的生物合成相结合，在任一生物合成途径中的突变体都大大损害了在非生物表面上的存活率。尽管海藻糖和α-葡聚糖都对非生物胁迫具有重要作用，但我们显示它们可以抵抗不同的胁迫。海藻糖对于PA01渗透胁迫反应至关重要，海藻糖合成突变体在盐分升高的条件下生长受到严重损害。但是，海藻糖并不能直接促进PA01的脱水反应。而是，脱水耐受性直接由源自GlgE的α-葡聚糖介导，而glgE合酶基因的缺失损害了PA01在低湿度下的存活，但对渗透敏感性的影响很小。干燥耐受性与海藻糖浓度无关，这标志着这两种分子在介导对非生物胁迫的响应中的作用之间有明显区别。干燥耐受性直接由源自GlgE的α-葡聚糖介导，glgE合酶基因的缺失损害了PA01在低湿度下的存活，但对渗透敏感性的影响很小。脱水耐受性与海藻糖浓度无关，这标志着这两种分子在介导对非生物胁迫的响应中的作用之间有明显区别。干燥耐受性直接由源自GlgE的α-葡聚糖介导，glgE合酶基因的缺失损害了PA01在低湿度下的存活，但对渗透敏感性的影响很小。脱水耐受性与海藻糖浓度无关，这标志着这两种分子在介导对非生物胁迫的响应中的作用之间有明显区别。