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缺失 BmoR 会影响脆弱拟杆菌中与硫醇/二硫键平衡相关基因的表达。

Deletion of BmoR affects the expression of genes related to thiol/disulfide balance in Bacteroides fragilis.

机构信息

Departamento de Microbiologia Médica, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.

出版信息

Sci Rep. 2018 Sep 26;8(1):14405. doi: 10.1038/s41598-018-32880-7.

DOI:10.1038/s41598-018-32880-7
PMID:30258073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6158253/
Abstract

Bacteroides fragilis, an opportunistic pathogen and commensal bacterium in the gut, is one the most aerotolerant species among strict anaerobes. However, the mechanisms that control gene regulation in response to oxidative stress are not completely understood. In this study, we show that the MarR type regulator, BmoR, regulates the expression of genes involved in the homeostasis of intracellular redox state. Transcriptome analysis showed that absence of BmoR leads to altered expression in total of 167 genes. Sixteen of these genes had a 2-fold or greater change in their expression. Most of these genes are related to LPS biosynthesis and carbohydrates metabolism, but there was a significant increase in the expression of genes related to the redox balance inside the cell. A pyridine nucleotide-disulfide oxidoreductase located directly upstream of bmoR was shown to be repressed by direct binding of BmoR to the promoter region. The expression of two other genes, coding for a thiosulphate:quinone-oxidoreductase and a thioredoxin, are indirectly affected by bmoR mutation during oxygen exposure. Phenotypic assays showed that BmoR is important to maintain the thiol/disulfide balance in the cell, confirming its relevance to B. fragilis response to oxidative stress.

摘要

脆弱拟杆菌是肠道中的机会致病菌和共生菌,是严格厌氧菌中最耐氧的物种之一。然而,控制基因调节以应对氧化应激的机制尚不完全清楚。在这项研究中,我们表明 MarR 型调节剂 BmoR 调节与细胞内氧化还原状态稳态相关的基因表达。转录组分析表明,BmoR 的缺失导致总共 167 个基因的表达发生改变。其中 16 个基因的表达有 2 倍或更大的变化。这些基因大多数与 LPS 生物合成和碳水化合物代谢有关,但与细胞内氧化还原平衡相关的基因表达显著增加。位于 bmoR 上游的吡啶核苷酸二硫化物氧化还原酶被证明可通过 BmoR 直接结合启动子区域而受到抑制。在暴露于氧气时,两个编码硫代硫酸盐:醌氧化还原酶和硫氧还蛋白的基因的表达受到 bmoR 突变的间接影响。表型测定表明,BmoR 对于维持细胞中的硫醇/二硫化物平衡很重要,这证实了它与 B. fragilis 对氧化应激的反应有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/8089440f08bc/41598_2018_32880_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/994262281613/41598_2018_32880_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/707556609d78/41598_2018_32880_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/24bacbe486b2/41598_2018_32880_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/37b1a8fd967d/41598_2018_32880_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/5924d48721af/41598_2018_32880_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/8089440f08bc/41598_2018_32880_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/994262281613/41598_2018_32880_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/707556609d78/41598_2018_32880_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/24bacbe486b2/41598_2018_32880_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/37b1a8fd967d/41598_2018_32880_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/5924d48721af/41598_2018_32880_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4054/6158253/8089440f08bc/41598_2018_32880_Fig6_HTML.jpg

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