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在使用CRISPR/Cas9介导的基因敲除进行代谢工程后,调控嘧啶生物合成的PyrR基因抗菌能力的丧失 。 (原句结尾处“in.”后面内容缺失,翻译可能不太完整准确)

Loss in the Antibacterial Ability of a PyrR Gene Regulating Pyrimidine Biosynthesis after Using CRISPR/Cas9-Mediated Knockout for Metabolic Engineering in .

作者信息

Chen Shaojun, He Xinmiao, Qin Ziliang, Li Gang, Wang Wentao, Nai Zida, Tian Yaguang, Liu Di, Jiang Xinpeng

机构信息

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.

Key Laboratory of Combining Farming and Animal Husbandry, Ministry of Agriculture, Animal Husbandry Research Institute, Heilongjiang Academy of Agricultural Sciences, No. 368 Xuefu Road, Harbin 150086, China.

出版信息

Microorganisms. 2023 Sep 22;11(10):2371. doi: 10.3390/microorganisms11102371.

DOI:10.3390/microorganisms11102371
PMID:37894029
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10609543/
Abstract

() has four possible mechanisms: antimicrobial antagonism, competitional adhesion, immunoregulation, and the inhibition of bacterial toxins. To delineate the metabolic reactions of nucleotides from that are associated with mechanisms of inhibiting pathogens and immunoregulation, we report that a PyrR-deficient strain was constructed using the CRISPR-Cas9 tool. Furthermore, there were some changes in its basic biological characterization, such as its growth curve, auxotroph, and morphological damage. The metabolic profiles of the supernatant between the PyrR-deficient and wild strains revealed the regulation of the synthesis of genetic material and of certain targeting pathways and metabolites. In addition, the characteristics of the PyrR-deficient strain were significantly altered as it lost the ability to inhibit the growth of pathogens. Moreover, we identified PyrR-regulating pyrimidine biosynthesis, which further improved its internalization and colocalization with macrophages. Evidence shows that the PyrR gene is a key active component in supernatants for the regulation of pyrimidine biosynthesis against a wide range of pathogens.

摘要

()有四种可能的机制:抗菌拮抗、竞争性黏附、免疫调节和抑制细菌毒素。为了描述与抑制病原体和免疫调节机制相关的核苷酸代谢反应,我们报告使用CRISPR-Cas9工具构建了一株PyrR缺陷型菌株。此外,其基本生物学特性发生了一些变化,如生长曲线、营养缺陷型和形态损伤。PyrR缺陷型菌株与野生型菌株之间的上清液代谢谱揭示了遗传物质合成以及某些靶向途径和代谢物的调控。此外,PyrR缺陷型菌株由于失去了抑制病原体生长的能力,其特性发生了显著改变。此外,我们鉴定出PyrR调节嘧啶生物合成,这进一步改善了其与巨噬细胞的内化和共定位。证据表明,PyrR基因是上清液中调节嘧啶生物合成以对抗多种病原体的关键活性成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/4131c372ac4d/microorganisms-11-02371-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/a4d78b04b55b/microorganisms-11-02371-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/a5b0f9c99e69/microorganisms-11-02371-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/f61d193170bc/microorganisms-11-02371-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/e9c8772b3c54/microorganisms-11-02371-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/ce472016fcd8/microorganisms-11-02371-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/bf694b2e82ab/microorganisms-11-02371-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/4131c372ac4d/microorganisms-11-02371-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/a4d78b04b55b/microorganisms-11-02371-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/a5b0f9c99e69/microorganisms-11-02371-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/f61d193170bc/microorganisms-11-02371-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/e9c8772b3c54/microorganisms-11-02371-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/ce472016fcd8/microorganisms-11-02371-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/bf694b2e82ab/microorganisms-11-02371-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3e2/10609543/4131c372ac4d/microorganisms-11-02371-g007.jpg

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