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采用多组学方法对幽门螺杆菌氧化还原开关 HP1021 调控组进行分析。

Profiling of the Helicobacter pylori redox switch HP1021 regulon using a multi-omics approach.

机构信息

Department of Microbiology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland.

Department of Molecular Microbiology, Faculty of Biotechnology, University of Wrocław, Wrocław, Poland.

出版信息

Nat Commun. 2023 Oct 23;14(1):6715. doi: 10.1038/s41467-023-42364-6.

DOI:10.1038/s41467-023-42364-6
PMID:37872172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10593804/
Abstract

The gastric human pathogen Helicobacter pylori has developed mechanisms to combat stress factors, including reactive oxygen species (ROS). Here, we present a comprehensive study on the redox switch protein HP1021 regulon combining transcriptomic, proteomic and DNA-protein interactions analyses. Our results indicate that HP1021 modulates H. pylori's response to oxidative stress. HP1021 controls the transcription of 497 genes, including 407 genes related to response to oxidative stress. 79 proteins are differently expressed in the HP1021 deletion mutant. HP1021 controls typical ROS response pathways (katA, rocF) and less canonical ones, particularly DNA uptake and central carbohydrate metabolism. HP1021 is a molecular regulator of competence in H. pylori, as HP1021-dependent repression of the comB DNA uptake genes is relieved under oxidative conditions, increasing natural competence. Furthermore, HP1021 controls glucose consumption by directly regulating the gluP transporter and has an important impact on maintaining the energetic balance in the cell.

摘要

胃病原体幽门螺杆菌已经开发出应对应激因素的机制,包括活性氧(ROS)。在这里,我们结合转录组、蛋白质组和 DNA-蛋白质相互作用分析,对氧化还原开关蛋白 HP1021 调控组进行了全面研究。我们的结果表明,HP1021 调节幽门螺杆菌对氧化应激的反应。HP1021 控制 497 个基因的转录,包括与应对氧化应激相关的 407 个基因。HP1021 缺失突变体中有 79 种蛋白质的表达水平不同。HP1021 控制典型的 ROS 反应途径(katA、rocF)和不太典型的途径,特别是 DNA 摄取和中心碳水化合物代谢。HP1021 是幽门螺杆菌感受态的分子调节剂,因为在氧化条件下,HP1021 依赖性抑制 comB DNA 摄取基因的作用得到缓解,从而增加了自然感受态。此外,HP1021 通过直接调节 gluP 转运蛋白来控制葡萄糖消耗,对维持细胞内的能量平衡有重要影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/4e32e0a9bbc8/41467_2023_42364_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/d4f18adafda6/41467_2023_42364_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/5397106b5f3c/41467_2023_42364_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/4e32e0a9bbc8/41467_2023_42364_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/d4f18adafda6/41467_2023_42364_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/5397106b5f3c/41467_2023_42364_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b413/10593804/4e32e0a9bbc8/41467_2023_42364_Fig3_HTML.jpg

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