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暴露于脱水-复水应激下的大肠杆菌中的蛋白质聚集和糖基化

Protein aggregation and glycation in Escherichia coli exposed to desiccation-rehydration stress.

作者信息

Łupkowska Adrianna, Monem Soroosh, Dębski Janusz, Stojowska-Swędrzyńska Karolina, Kuczyńska-Wiśnik Dorota, Laskowska Ewa

机构信息

Department of General and Medical Biochemistry, Faculty of Biology, University of Gdansk, Wita Stwosza 59, 80-308 Gdansk, Poland.

Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawińskiego 5a, 02-106 Warsaw, Poland.

出版信息

Microbiol Res. 2023 May;270:127335. doi: 10.1016/j.micres.2023.127335. Epub 2023 Feb 16.

DOI:10.1016/j.micres.2023.127335
PMID:36841129
Abstract

In natural environments, bacteria often enter a state of anhydrobiosis due to water loss. Multiple studies have demonstrated that desiccation may lead to protein aggregation and glycation both in vivo and in vitro. However, the exact effects of water-loss-induced proteotoxic stress and the interplay between protein glycation and aggregation in bacteria remain elusive. Our studies revealed that protein aggregates formation in Escherichia coli started during desiccation and continued during the rehydration stage. The aggregates were enriched in proteins prone to liquid-liquid phase separation. Although it is known that glycation may induce protein aggregation in vitro, the aggregates formed in E. coli contained low levels of glycation products compared to the soluble protein fraction. Carnosine, glycine betaine and trehalose diminished the formation of protein aggregates and glycation products, resulting in increased E. coli viability. Notably, although high concentrations of glycine-betaine and trehalose significantly enhanced protein aggregation, glycation was still inhibited and E. coli cells survived desiccation better than bacteria grown without osmolytes. Taken together, our results suggest that the aggregates might play protective functions during early desiccation-rehydration stress. Moreover, it seems glycation rather than protein aggregation is the main cause of E. coli death upon desiccation-rehydration stress.

摘要

在自然环境中,细菌常因水分流失而进入脱水休眠状态。多项研究表明,干燥在体内和体外均可导致蛋白质聚集和糖基化。然而,水分流失诱导的蛋白质毒性应激的确切影响以及细菌中蛋白质糖基化与聚集之间的相互作用仍不清楚。我们的研究表明,大肠杆菌中的蛋白质聚集体在干燥过程中开始形成,并在复水阶段持续存在。这些聚集体富含易于发生液-液相分离的蛋白质。虽然已知糖基化在体外可能诱导蛋白质聚集,但与可溶性蛋白质部分相比,大肠杆菌中形成的聚集体含有低水平的糖基化产物。肌肽、甘氨酸甜菜碱和海藻糖减少了蛋白质聚集体和糖基化产物的形成,从而提高了大肠杆菌的存活率。值得注意的是,虽然高浓度的甘氨酸甜菜碱和海藻糖显著增强了蛋白质聚集,但糖基化仍受到抑制,并且与未添加渗透保护剂培养的细菌相比,大肠杆菌细胞在干燥后存活得更好。综上所述,我们的结果表明,聚集体可能在早期脱水-复水应激期间发挥保护作用。此外,似乎糖基化而非蛋白质聚集是大肠杆菌在脱水-复水应激后死亡的主要原因。

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