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所获得的基因簇介导对铜的抗性。

The acquired gene cluster in mediates resistance to copper.

作者信息

Hikal Ahmed F, Hasan Sameer, Gudeta Dereje, Zhao Shaohua, Foley Steven, Khan Ashraf A

机构信息

Division of Microbiology, National Center for Toxicological Research, United States Food and Drug Administration, Jefferson, AR, United States.

Office of Applied Science, Center for Veterinary Medicine, U.S. Food and Drug Administration, Laurel, MD, United States.

出版信息

Front Microbiol. 2024 Sep 3;15:1454763. doi: 10.3389/fmicb.2024.1454763. eCollection 2024.

DOI:10.3389/fmicb.2024.1454763
PMID:39290517
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11406079/
Abstract

The pervasive environmental metal contamination has led to selection of heavy-metal resistance genes in bacteria. The and clusters are located on a mobile genetic element and linked to heavy-metal resistance. These clusters have been found in serovars isolated from human clinical cases and foods of animal origin. This may be due to the use of heavy metals, such as copper, in animal feed for their antimicrobial and growth promotion properties. The cluster can be found alone or in combination with cluster, either in the chromosome or on a plasmid. Previous reports have indicated that , but not cluster contributes to copper resistance in Typhimurium. However, the role of the cluster on the physiology of non-typhoidal remains poorly understood. To understand the function of the gene cluster, a deletion mutant of genes was constructed using allelic exchange mutagenesis. Deletion of genes inhibited growth of in high-copper medium, but only under anaerobic environment. Complementation of the mutant reversed the growth phenotype. The survival of in RAW264.7 macrophages was not affected by the loss of genes. This study indicates that the acquired cluster is crucial for copper detoxification in , but it is not essential for intracellular replication within macrophages.

摘要

普遍存在的环境金属污染导致细菌中重金属抗性基因的选择。某簇基因位于一个可移动遗传元件上,并与重金属抗性相关。这些基因簇已在从人类临床病例和动物源性食品中分离出的某些血清型中发现。这可能是由于在动物饲料中使用了铜等重金属,因其具有抗菌和促进生长的特性。该基因簇可以单独存在,也可以与另一簇基因一起存在于染色体或质粒上。先前的报告表明,在鼠伤寒沙门氏菌中,某簇基因(而非另一簇基因)有助于铜抗性。然而,另一簇基因在非伤寒沙门氏菌生理学上的作用仍知之甚少。为了了解该基因簇的功能,利用等位基因交换诱变构建了该基因簇的缺失突变体。该基因簇的缺失抑制了沙门氏菌在高铜培养基中的生长,但仅在厌氧环境下如此。突变体的互补作用逆转了生长表型。沙门氏菌在RAW264.7巨噬细胞中的存活不受该基因簇缺失的影响。这项研究表明,获得的该基因簇对沙门氏菌中的铜解毒至关重要,但对于在巨噬细胞内的细胞内复制并非必不可少。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/6172fe6e03b3/fmicb-15-1454763-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/bfd5794700d4/fmicb-15-1454763-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/88cdf913fd16/fmicb-15-1454763-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/044941cc9341/fmicb-15-1454763-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/be670bdf9cf1/fmicb-15-1454763-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/8eba2dd0ae6e/fmicb-15-1454763-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/6172fe6e03b3/fmicb-15-1454763-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/bfd5794700d4/fmicb-15-1454763-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/88cdf913fd16/fmicb-15-1454763-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/044941cc9341/fmicb-15-1454763-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/be670bdf9cf1/fmicb-15-1454763-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/8eba2dd0ae6e/fmicb-15-1454763-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da99/11406079/6172fe6e03b3/fmicb-15-1454763-g006.jpg

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