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转座子定向插入位点测序揭示糖酵解基因是HO防御机制的一部分。 (原英文文本结尾处“in.”后缺少具体内容,翻译只能根据现有内容尽量准确表述)

Transposon-Directed Insertion-Site Sequencing Reveals Glycolysis Gene as Part of the HO Defense Mechanisms in .

作者信息

Roth Myriam, Goodall Emily C A, Pullela Karthik, Jaquet Vincent, François Patrice, Henderson Ian R, Krause Karl-Heinz

机构信息

Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, 1211 Geneva, Switzerland.

Institute for Molecular Bioscience, University of Queensland, St. Lucia, Brisbane, QLD 4072, Australia.

出版信息

Antioxidants (Basel). 2022 Oct 18;11(10):2053. doi: 10.3390/antiox11102053.

DOI:10.3390/antiox11102053
PMID:36290776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9598634/
Abstract

Hydrogen peroxide (HO) is a common effector of defense mechanisms against pathogenic infections. However, bacterial factors involved in HO tolerance remain unclear. Here we used transposon-directed insertion-site sequencing (TraDIS), a technique allowing the screening of the whole genome, to identify genes implicated in HO tolerance in . Our TraDIS analysis identified 10 mutants with fitness defect upon HO exposure, among which previously HO-associated genes (, , , , and ) and other genes with no known association with HO tolerance in (, , and ). This is the first description of the impact of , a gene involved in glycolysis, on the susceptibility of to HO. Indeed, confirmatory experiments showed that the deletion of led to a specific hypersensitivity to HO comparable to the deletion of the major HO scavenger gene . This hypersensitivity was not due to an alteration of catalase function and was independent of the carbon source or the presence of oxygen. Transcription of was upregulated under HO exposure, highlighting its role under oxidative stress. In summary, our TraDIS approach identified as a member of the oxidative stress defense mechanism in .

摘要

过氧化氢(HO)是抵御病原体感染的防御机制中的常见效应分子。然而,参与耐受HO的细菌因子仍不清楚。在此,我们使用转座子导向插入位点测序(TraDIS),一种能够筛选全基因组的技术,来鉴定在[具体细菌名称未给出]中与耐受HO相关的基因。我们的TraDIS分析鉴定出10个在HO暴露后具有适应性缺陷的突变体,其中包括先前与HO相关的基因([具体基因名称未给出])以及在[具体细菌名称未给出]中其他与耐受HO无已知关联的基因([具体基因名称未给出])。这是首次描述参与糖酵解的基因[具体基因名称未给出]对[具体细菌名称未给出]对HO敏感性的影响。的确,验证性实验表明,[具体基因名称未给出]的缺失导致对HO的特异性超敏反应,与主要HO清除基因[具体基因名称未给出]的缺失相当。这种超敏反应不是由于过氧化氢酶功能的改变,并且与碳源或氧气的存在无关。在HO暴露下,[具体基因名称未给出]的转录上调,突出了其在氧化应激下的作用。总之,我们的TraDIS方法鉴定出[具体基因名称未给出]是[具体细菌名称未给出]氧化应激防御机制的成员。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/95bbb6873b49/antioxidants-11-02053-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/44ec233d2717/antioxidants-11-02053-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/0f8599e1c94a/antioxidants-11-02053-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/e43d7318a528/antioxidants-11-02053-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/da0c2c295acc/antioxidants-11-02053-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/ce2831b35218/antioxidants-11-02053-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/7c70f42a87d9/antioxidants-11-02053-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/95bbb6873b49/antioxidants-11-02053-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/44ec233d2717/antioxidants-11-02053-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/0f8599e1c94a/antioxidants-11-02053-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/e43d7318a528/antioxidants-11-02053-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/da0c2c295acc/antioxidants-11-02053-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/ce2831b35218/antioxidants-11-02053-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/7c70f42a87d9/antioxidants-11-02053-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bcf/9598634/95bbb6873b49/antioxidants-11-02053-g007.jpg

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