Scholarlink

<p>Plasmids play a major role in the spread of antibiotic resistance genes in bacteria. Plasmid copy number (PCN) is often tightly regulated. In plasmids of the ColE1-type, this regulation happens by a negative feedback mechanism using an antisense RNA. Here, we employed a sequencing-based method for determining PCN to demonstrate that copy number of different ColE1-family plasmids harboring antibiotic resistance genes increases during antibiotic treatment. Further, we show that deletion of the gene <i>pcnB</i> reduces the copy number of ColE1-family plasmids in <i>E. coli</i> MG1655, which in turn results in a reduced resistance to antimicrobials of the classes aminoglycosides, β-lactams and tetracyclines. In the absence of antibiotic selection, the deletion of <i>pcnB</i> also decreased the number of ColE1-type plasmids in a bacterial population. Hence, PcnB, which polyadenylates RNA, marking it for decay, represents a potential drug and helper-drug target that could be used to reduce PCN to re-sensitize bacteria with multi-copy-number resistance-plasmids to treatment with different antimicrobials.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Deletion of pcnB affects antibiotic susceptibility in resistant Escherichia coli by reducing copy number of ColE1-family plasmids

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月11日

查看全文
  • Sandra Marina Wellner,
  • Xiao Fei,
  • Ana Herrero-Fresno,
  • John Elmerdahl Olsen

摘要

Plasmids play a major role in the spread of antibiotic resistance genes in bacteria. Plasmid copy number (PCN) is often tightly regulated. In plasmids of the ColE1-type, this regulation happens by a negative feedback mechanism using an antisense RNA. Here, we employed a sequencing-based method for determining PCN to demonstrate that copy number of different ColE1-family plasmids harboring antibiotic resistance genes increases during antibiotic treatment. Further, we show that deletion of the gene pcnB reduces the copy number of ColE1-family plasmids in E. coli MG1655, which in turn results in a reduced resistance to antimicrobials of the classes aminoglycosides, β-lactams and tetracyclines. In the absence of antibiotic selection, the deletion of pcnB also decreased the number of ColE1-type plasmids in a bacterial population. Hence, PcnB, which polyadenylates RNA, marking it for decay, represents a potential drug and helper-drug target that could be used to reduce PCN to re-sensitize bacteria with multi-copy-number resistance-plasmids to treatment with different antimicrobials.