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在 Alginate 降解弧菌中揭示了单靶点调控因子 NorR 参与群集运动和生物膜形成的新功能。

Novel function of single-target regulator NorR involved in swarming motility and biofilm formation revealed in Vibrio alginolyticus.

机构信息

Department of Biology, Shantou University, Shantou, Guangdong, 515063, China.

Dongguan Nancheng Business District North School, Dongguan, 523000, China.

出版信息

BMC Biol. 2024 Nov 6;22(1):253. doi: 10.1186/s12915-024-02057-y.

Abstract

NorR, as a single-target regulator, has been demonstrated to be involved in NO detoxification in bacteria under anaerobic conditions. Here, the norR gene was identified and deleted in the genome of Vibrio alginolyticus. The results showed that deletion of norR in Vibrio alginolyticus led to lower swarming motility and more biofilm formation on aerobic condition. Moreover, we proved that NorR from E. coli had a similar function in controlling motility. NorR overexpression led to increased resistance to oxidative stress and tetracycline. We also observed a reduced ability of the NorR-overexpressing strain to adapt to iron limitation condition. Transcriptome analysis showed that the genes responsible for bacterial motility and biofilm formation were affected by NorR. The expressions of several sigma factors (RpoS, RpoN, and RpoH) and response regulators (LuxR and MarR) were also controlled by NorR. Furthermore, Chip-qPCR showed that there is a direct binding between NorR and the promoter of rpoS. Based on these results, NorR appears to be a central regulator involved in biofilm formation and swarming motility in Vibrio alginolyticus.

摘要

NorR 作为一种单一靶点的调节剂,已被证明参与了厌氧菌中 NO 的解毒。在此,我们在副溶血弧菌基因组中鉴定并删除了 norR 基因。结果表明,副溶血弧菌中 norR 的缺失导致有氧条件下的群集运动能力降低和生物膜形成增多。此外,我们证明了大肠杆菌中的 NorR 具有类似的控制运动能力的功能。NorR 的过表达导致对氧化应激和四环素的抗性增加。我们还观察到 NorR 过表达菌株适应铁限制条件的能力降低。转录组分析表明,与细菌运动和生物膜形成有关的基因受到 NorR 的影响。几种 sigma 因子(RpoS、RpoN 和 RpoH)和响应调节剂(LuxR 和 MarR)的表达也受到 NorR 的控制。此外,Chip-qPCR 表明 NorR 与 rpoS 启动子之间存在直接结合。基于这些结果,NorR 似乎是参与副溶血弧菌生物膜形成和群集运动的核心调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2215/11542441/3ef958cd75d3/12915_2024_2057_Fig1_HTML.jpg

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