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cAMP - CRP激活在应激条件下导致生长停滞。

cAMP-CRP-activated causes growth arrest under stress conditions.

作者信息

Haque Most Farzana, Tarusawa Takefusa, Ushida Chisato, Ito Shion, Himeno Hyouta

机构信息

Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki, Japan.

The United Graduate School of Agricultural Sciences, Iwate University, Morioka, Japan.

出版信息

Front Microbiol. 2025 Aug 29;16:1597530. doi: 10.3389/fmicb.2025.1597530. eCollection 2025.

Abstract

Cells are exposed to various kinds of stress, obliging them to cope with the challenges they encounter. Upon subjecting cells to oxidative stress induced by elevated concentrations of hydrogen peroxide or plumbagin, as well as osmotic stress by elevated NaCl concentrations, cell growth stopped immediately after stress and it resumed after a period of time. In the present study, we found that the stress-induced growth arrest disappeared when the gene for cAMP synthesis () or its receptor protein () was deleted, whereas it reappeared when cAMP is exogenously added to cells. With increasing stress intensity, the period of growth arrest increased in the wild-type cells, while or cells continued to grow without arrest, although their growth rates were reduced. These results indicate that cell has a novel cAMP-CRP-dependent mechanism to stop cell growth temporarily for adaptation to new environment when subjected to a strong stress, whether oxidative or osmotic stress.

摘要

细胞会受到各种应激,这迫使它们应对所遇到的挑战。当细胞受到过氧化氢或白花丹素浓度升高诱导的氧化应激以及氯化钠浓度升高引起的渗透应激时,应激后细胞生长立即停止,一段时间后恢复。在本研究中,我们发现当cAMP合成基因()或其受体蛋白()被删除时,应激诱导的生长停滞消失,而当向细胞中添加外源性cAMP时,生长停滞又会重新出现。随着应激强度的增加,野生型细胞的生长停滞期延长,而或细胞虽生长速率降低但继续生长而不发生停滞。这些结果表明,细胞具有一种新的cAMP - CRP依赖性机制,在受到强烈应激(无论是氧化应激还是渗透应激)时,会暂时停止细胞生长以适应新环境。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f29d/12426135/a11d75459116/fmicb-16-1597530-g001.jpg

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