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组学研究揭示了[具体对象]对L-高丝氨酸渗透胁迫的响应机制。 (原文中“of”后面缺少具体内容)

Omics studies reveal the response mechanisms of to l-homoserine osmotic stress.

作者信息

Wang Jian, Lin Yicun, Yang Jian, Chen Yuxiang, Xu Ning, Liu Jun, Sun Wei, Li Dawei

机构信息

College of Biological and Agricultural Engineering, Jilin University, Changchun, 130022 China.

Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences, Tianjin, 300308 China.

出版信息

3 Biotech. 2025 May;15(5):127. doi: 10.1007/s13205-025-04304-7. Epub 2025 Apr 16.

DOI:10.1007/s13205-025-04304-7
PMID:40255446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12003223/
Abstract

UNLABELLED

To investigate the mechanism of osmotic stress produced by in the production of l-homoserine The present study employed genomic and transcriptomic analyses of both evolved strains and the parental strain grown under l-homoserine osmotic stress to investigate the response mechanisms and identify specific tolerance targets. The results indicated that the evolved strain enhanced its tolerance to l-homoserine stress by inactivating aspartokinase, thereby interrupting the intracellular synthesis pathway of l-homoserine. Early in stress exposure, suppressed the synthesis of l -homoserine and instead enhanced its catabolic activity. In response to osmotic stress, also relied on a variety of energy metabolism and ion transport pathways, including ABC transporters and ATP metabolism, which are essential for high-osmolarity tolerance. Given the gradual accumulation of l-homoserine within the cell, this study focused on the transcriptional expression patterns during the adaptation phase, excluding cellular responses during the high-concentration stress phase. These findings provide valuable insights for improving 's tolerance to l-homoserine stress during amino-acid fermentation and highlight potential targets for metabolic engineering strategies.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s13205-025-04304-7.

摘要

未标记

为了研究l-高丝氨酸生产过程中渗透压应激产生的机制,本研究对在l-高丝氨酸渗透压应激下生长的进化菌株和亲本菌株进行了基因组和转录组分析,以研究其响应机制并确定特定的耐受靶点。结果表明,进化菌株通过使天冬氨酸激酶失活来增强其对l-高丝氨酸应激的耐受性,从而中断了l-高丝氨酸的细胞内合成途径。在应激暴露早期,抑制了l-高丝氨酸的合成,反而增强了其分解代谢活性。为了应对渗透压应激,还依赖于多种能量代谢和离子转运途径,包括ABC转运蛋白和ATP代谢,这些对于高渗透压耐受性至关重要。鉴于l-高丝氨酸在细胞内的逐渐积累,本研究重点关注适应阶段的转录表达模式,排除了高浓度应激阶段的细胞反应。这些发现为提高氨基酸发酵过程中对l-高丝氨酸应激的耐受性提供了有价值的见解,并突出了代谢工程策略的潜在靶点。

补充信息

在线版本包含可在10.1007/s13205-025-04304-7获取的补充材料。

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