Desiccation is a common stress that bacteria face in the natural environment, and thus, they have developed a variety of protective mechanisms to mitigate the damage caused by water loss. The formation of biofilms and the accumulation of trehalose and sporulation are well-known strategies used by bacteria to survive desiccation. Other mechanisms, including intrinsically disordered proteins and the anti-glycation defence, have been mainly studied in eukaryotic cells, and their role in bacteria remains unclear. We have recently shown that the impairment of trehalose synthesis results in higher glucose availability, leading to the accumulation of acetyl phosphate and enhanced protein acetylation, which in turn stimulates protein aggregation. In the absence of trehalose synthesis, excess glucose may stimulate non-enzymatic glycosylation and the formation of advanced glycation end products (AGEs) bound to proteins. Therefore, we propose that trehalose may prevent protein damage, not only as a chemical chaperone but also as a metabolite that indirectly counteracts detrimental protein acetylation and glycation.

中文翻译：

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干燥过程中保护细菌的机制的新见解。

干燥是细菌在自然环境中面临的普遍压力，因此，它们已开发出多种保护机制来减轻因水分流失而造成的损害。生物膜的形成以及海藻糖的积累和孢子形成是细菌在干燥过程中生存所采用的众所周知的策略。主要在真核细胞中研究了其他机制，包括内在无序的蛋白质和抗糖基化防御，其在细菌中的作用仍不清楚。我们最近显示，海藻糖合成的损害导致更高的葡萄糖利用率，导致乙酰磷酸的积累和增强的蛋白质乙酰化，进而刺激蛋白质聚集。在没有海藻糖合成的情况下，过量的葡萄糖可能会刺激非酶糖基化，并形成与蛋白质结合的高级糖基化终产物（AGEs）。因此，我们提出海藻糖不仅可以作为化学分子伴侣，而且可以作为间接抵消有害蛋白质乙酰化和糖基化的代谢产物来预防蛋白质损伤。