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氧化型OxyR上调表达以抑制超氧化物歧化酶和过氧化氢酶缺陷菌株的平板接种缺陷。

Oxidized OxyR Up-Regulates Expression to Suppress Plating Defects of and Catalase-Deficient Strains.

作者信息

Wan Fen, Yin Jianhua, Sun Weining, Gao Haichun

机构信息

College of Laboratory Medicine, Hangzhou Medical College, Hangzhou, China.

College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou, China.

出版信息

Front Microbiol. 2019 Mar 7;10:439. doi: 10.3389/fmicb.2019.00439. eCollection 2019.

DOI:10.3389/fmicb.2019.00439
PMID:30899252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6416212/
Abstract

It is well established that in bacteria, such as , OxyR is a transcriptional regulator that mediates the response to HO by activating the OxyR regulon, which consists of many genes that play vital roles in oxidative stress resistance. In , OxyR regulates, however, in both reduced and oxidized states, the production of HO scavengers, including major catalase KatB and NADH peroxidase AhpCF. Here we showed that the mutant carried a plating defect manifested as division arresting, a phenotype that can be completely suppressed by an OxyR variant constitutively existing in oxidized form (OxyR). This effect of OxyR could not be solely attributed to the increment in KatB production, since the suppression was also observed in the absence of KatB. Although expression of peroxidase CcpA was greatly activated by OxyR, the contribution of the protein in alleviating plating defect was negligible. We eventually identified AhpCF as the critical factor, when produced at substantially elevated levels by OxyR, to protect the cell from HO attack. Our data indicate that AhpCF is a particularly important peroxidase in oxidative stress resistance in , not only playing a compensatory role for catalase, but also by itself providing sufficient protection from killing of HO generated abiotically.

摘要

众所周知,在诸如大肠杆菌等细菌中,OxyR是一种转录调节因子,它通过激活OxyR调控子来介导对过氧化氢(HO)的应答,该调控子由许多在抗氧化应激中起关键作用的基因组成。然而,在大肠杆菌中,无论处于还原态还是氧化态,OxyR都能调节HO清除剂的产生,包括主要的过氧化氢酶KatB和NADH过氧化物酶AhpCF。在这里我们表明,某突变体存在平板缺陷,表现为分裂停滞,而这种表型可以被一种以氧化形式组成型存在的OxyR变体(OxyR*)完全抑制。OxyR的这种作用不能仅仅归因于KatB产量的增加,因为在没有KatB的情况下也观察到了这种抑制作用。尽管过氧化物酶CcpA的表达被OxyR极大地激活,但该蛋白在减轻平板缺陷方面的作用可以忽略不计。我们最终确定AhpCF是关键因素,当OxyR使其大量表达时,它能保护细胞免受HO的攻击。我们的数据表明,AhpCF在大肠杆菌的抗氧化应激中是一种特别重要的过氧化物酶,不仅对过氧化氢酶起到补偿作用,而且自身就能为抵御非生物产生的HO的杀伤提供足够的保护。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/fca18aa9ec50/fmicb-10-00439-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/4cebd20bba34/fmicb-10-00439-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/4c7e54896c05/fmicb-10-00439-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/e8c57f6af3e2/fmicb-10-00439-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/fca18aa9ec50/fmicb-10-00439-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/4cebd20bba34/fmicb-10-00439-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/4c7e54896c05/fmicb-10-00439-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/e8c57f6af3e2/fmicb-10-00439-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738a/6416212/fca18aa9ec50/fmicb-10-00439-g004.jpg

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