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烷烃磺酸盐单加氧酶在氧化应激下的保护作用。

Protective Role of Bacterial Alkanesulfonate Monooxygenase under Oxidative Stress.

机构信息

Laboratory of Molecular Environmental Microbiology, Department of Environmental Science and Ecological Engineering, Korea University, Seoul, South Korea.

Laboratory of Molecular Environmental Microbiology, Department of Environmental Science and Ecological Engineering, Korea University, Seoul, South Korea

出版信息

Appl Environ Microbiol. 2020 Jul 20;86(15). doi: 10.1128/AEM.00692-20.

DOI:10.1128/AEM.00692-20
PMID:32503904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7376545/
Abstract

Bacterial alkane metabolism is associated with a number of cellular stresses, including membrane stress and oxidative stress, and the limited uptake of charged ions such as sulfate. In the present study, the genes and in DR1 cells, which encode an alkanesulfonate monooxygenase and a taurine dioxygenase, respectively, were found to be responsible for hexadecanesulfonate (CSOH) and taurine metabolism, and Cbl was experimentally identified as a potential regulator of and expression. The expression of and occurred under sulfate-limited conditions generated during -hexadecane degradation. Interestingly, expression analysis and knockout experiments suggested that both genes are required to protect cells against oxidative stress, including that generated by -hexadecane degradation and HO exposure. Measurable levels of intracellular hexadecanesulfonate were also produced during -hexadecane degradation. Phylogenetic analysis suggested that and are mainly present in soil-dwelling aerobes within the and classes, which suggests that they function as controllers of the sulfur cycle and play a protective role against oxidative stress in sulfur-limited conditions. and , which play a role in the degradation of organosulfonate, were expressed during -hexadecane metabolism and oxidative stress conditions in DR1. Our study confirmed that hexadecanesulfonate was accidentally generated during bacterial -hexadecane degradation in sulfate-limited conditions. Removal of this by-product by SsuD and TauD must be necessary for bacterial survival under oxidative stress generated during -hexadecane degradation.

摘要

细菌烷烃代谢与许多细胞应激有关,包括膜应激和氧化应激,以及有限的带电荷离子(如硫酸盐)的摄取。在本研究中,发现 DR1 细胞中的基因 和 分别编码烷磺酸盐单加氧酶和牛磺酸双加氧酶,负责十六烷磺酸盐(CSOH)和牛磺酸代谢,并且 Cbl 被实验鉴定为 和 表达的潜在调节剂。在 -十六烷降解过程中产生的硫酸盐有限条件下, 和 的表达发生。有趣的是,表达分析和敲除实验表明,这两个基因都需要保护细胞免受氧化应激,包括 -十六烷降解和 HO 暴露产生的氧化应激。在 -十六烷降解过程中也产生了可测量水平的细胞内十六烷磺酸盐。系统发育分析表明, 和 主要存在于土壤中需氧的 和 类细菌中,这表明它们作为硫循环的控制器发挥作用,并在硫有限条件下对氧化应激起到保护作用。在 -十六烷代谢和 DR1 中的氧化应激条件下表达了 和 ,它们在有机磺酸盐的降解中起作用。我们的研究证实,在硫酸盐有限条件下,细菌 -十六烷降解过程中意外生成了十六烷磺酸盐。在 -十六烷降解过程中产生的氧化应激下,SsuD 和 TauD 必须去除这种副产物,这对细菌的生存是必要的。

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