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LM1001中的耐酸性反应及其机制。

Acid tolerance responses and their mechanisms in LM1001.

作者信息

Lee Min-Gyu, Kang Min Joo, Cha Soyoung, Kim Tae-Rahk, Park Young-Seo

机构信息

Department of Food Science and Biotechnology, Gachon University, Seongnam, 13120 Republic of Korea.

Lactomason Co., Ltd, Jinju, 52840 Republic of Korea.

出版信息

Food Sci Biotechnol. 2024 Jun 4;33(9):2213-2222. doi: 10.1007/s10068-024-01582-4. eCollection 2024 Jul.

Abstract

UNLABELLED

This study investigated the acid tolerance responses of LM1001 at physiological and molecular levels. Upon exposure to low pH, LM1001 demonstrated increased ATPase activity and ammonia consumption, which contributed to a higher intracellular pH. Comparative analysis of cell membrane fatty acids revealed that acid-stressed cells had a significantly higher proportion of unsaturated fatty acids than those of unstressed cells. There was differential upregulation of several genes, notably those involved in alkali production ( and ) and in class I and class III stress responses ( and ). Following 2-h exposure to pH 2.5, LM1001 not only exhibited enhanced survival but also showed increased auto-aggregation and improved mucin adhesion capability, albeit with a reduction in hydrophobicity. These findings indicate that acid stress induces adaptive physiological and metabolic changes in LM1001, enhancing its acid resistance and adherence properties.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10068-024-01582-4.

摘要

未标注

本研究在生理和分子水平上研究了LM1001的耐酸性反应。暴露于低pH值环境时,LM1001表现出ATP酶活性增加和氨消耗增加,这有助于提高细胞内pH值。细胞膜脂肪酸的比较分析表明,酸胁迫细胞中不饱和脂肪酸的比例明显高于未受胁迫的细胞。几个基因存在差异上调,特别是那些参与碱产生(和)以及I类和III类应激反应(和)的基因。在pH 2.5条件下暴露2小时后,LM1001不仅存活率提高,而且自聚集增加,粘蛋白粘附能力提高,尽管疏水性有所降低。这些发现表明,酸胁迫会诱导LM1001发生适应性生理和代谢变化,增强其耐酸性和粘附特性。

补充信息

在线版本包含可在10.1007/s10068-024-01582-4获取的补充材料。

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