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缺失红杆菌丝氨酸乙酰基转移酶基因, , 可损害基因转移剂和生物膜表型的基因转移。

Loss of the Rhodobacter capsulatus Serine Acetyl Transferase Gene, , Impairs Gene Transfer by Gene Transfer Agents and Biofilm Phenotypes.

机构信息

Biology Department, University of Yorkgrid.5685.e, York, United Kingdom.

York Biomedical Research Institute, University of Yorkgrid.5685.e, York, United Kingdom.

出版信息

Appl Environ Microbiol. 2022 Oct 11;88(19):e0094422. doi: 10.1128/aem.00944-22. Epub 2022 Sep 13.

DOI:10.1128/aem.00944-22
PMID:36098534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9552610/
Abstract

Biofilms are widespread in the environment, where they allow bacterial species to survive adverse conditions. Cells in biofilms are densely packed, and this proximity is likely to increase the frequency of horizontal gene transfer. Gene transfer agents (GTAs) are domesticated viruses with the potential to spread any gene between bacteria. GTA production is normally restricted to a small subpopulation of bacteria, and regulation of GTA loci is highly coordinated, but the environmental conditions that favor GTA production are poorly understood. Here, we identified a serine acetyltransferase gene, , in Rhodobacter capsulatus that is required for optimal receipt of GTA DNA, accumulation of extracellular polysaccharide, and biofilm formation. The gene is directly downstream of the core -like GTA (RcGTA) structural gene cluster and upregulated in an RcGTA overproducer strain, although it is expressed on a separate transcript. The data we present suggest that GTA production and biofilm are coregulated, which could have important implications for the study of rapid bacterial evolution and understanding the full impact of GTAs in the environment. Direct exchange of genes between bacteria leads to rapid evolution and is the major factor underlying the spread of antibiotic resistance. Gene transfer agents (GTAs) are an unusual but understudied mechanism for genetic exchange that are capable of transferring any gene from one bacterium to another, and therefore, GTAs are likely to be important factors in genome plasticity in the environment. Despite the potential impact of GTAs, our knowledge of their regulation is incomplete. In this paper, we present evidence that elements of the cysteine biosynthesis pathway are involved in coregulation of various phenotypes required for optimal biofilm formation by Rhodobacter capsulatus and successful infection by the archetypal RcGTA. Establishing the regulatory mechanisms controlling GTA-mediated gene transfer is a key stepping stone to allow a full understanding of their role in the environment and wider impact.

摘要

生物膜广泛存在于环境中,使细菌能够在不利条件下生存。生物膜中的细胞密集排列,这可能会增加水平基因转移的频率。基因转移因子 (GTAs) 是具有在细菌之间传播任何基因潜力的驯化病毒。GTA 的产生通常仅限于一小部分细菌,并且 GTA 基因座的调控高度协调,但有利于 GTA 产生的环境条件知之甚少。在这里,我们在荚膜红细菌中鉴定了一个丝氨酸乙酰转移酶基因 ,该基因对于最佳接收 GTA DNA、积累细胞外多糖和生物膜形成是必需的。 基因位于核心样 GTA (RcGTA) 结构基因簇的下游,并且在 RcGTA 过表达菌株中上调,尽管它在单独的转录本上表达。我们提出的这些数据表明,GTA 的产生和生物膜是共调控的,这对于快速细菌进化的研究和理解 GTAs 在环境中的全部影响具有重要意义。细菌之间基因的直接交换导致快速进化,是抗生素耐药性传播的主要因素。基因转移因子 (GTAs) 是一种不寻常但研究不足的遗传交换机制,能够将任何基因从一种细菌转移到另一种细菌,因此,GTAs 很可能是环境中基因组可塑性的重要因素。尽管 GTAs 具有潜在影响,但我们对它们的调控知之甚少。在本文中,我们提供的证据表明,半胱氨酸生物合成途径的元件参与了荚膜红细菌最佳生物膜形成和典型 RcGTA 成功感染所需的各种表型的协同调控。建立控制 GTA 介导的基因转移的调控机制是全面理解它们在环境中的作用及其更广泛影响的关键步骤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/5cf095e31922/aem.00944-22-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/3aadb9f74e9c/aem.00944-22-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/c6e0ef489b4c/aem.00944-22-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/f6c9e130d99b/aem.00944-22-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/6e4e5986e175/aem.00944-22-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/25d3aa6ab49a/aem.00944-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/efa4fd7951b3/aem.00944-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/49783c4f3cde/aem.00944-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/5cf095e31922/aem.00944-22-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/3aadb9f74e9c/aem.00944-22-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/c6e0ef489b4c/aem.00944-22-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/f6c9e130d99b/aem.00944-22-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/6e4e5986e175/aem.00944-22-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/25d3aa6ab49a/aem.00944-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/efa4fd7951b3/aem.00944-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/49783c4f3cde/aem.00944-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3405/9552610/5cf095e31922/aem.00944-22-f008.jpg

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