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<p>Antimicrobial peptides (AMPs) play important roles in suppressing bacterial colonization and infection, and several AMPs are used as antimicrobial agents. Conversely, bacteria possess mechanisms that confer resistance to AMPs. We previously identified clinical <i>Staphylococcus aureus</i> isolates lacking the <i>vraDEH</i> genes, which are involved in nisin and bacitracin resistance. All such isolates belonged to clonal complex (CC) 121 and exhibited increased susceptibility to nisin A and bacitracin. The absence of <i>vraDEH</i> was accompanied by the absence of a 35,005-bp genomic region encompassing the biofilm-associated <i>icaRADBC</i> genes and a histidine biosynthesis operon. In a <i>vraDEH</i>-positive CC121 strain, this region was flanked by two IS<i>1181</i> elements, whereas in <i>vraDEH</i>-negative strains it was replaced by a single IS<i>1181</i> element, suggesting deletion through recombination between IS elements. Analysis of publicly available genomes revealed that all strains carrying the 35-kb deletion belonged to a single phylogenetic subclade of CC121. The downstream IS<i>1181</i> insertion was frequently found in CC121 strains, whereas the upstream insertion was only found in this subclade. Across the <i>S. aureus</i> population, IS<i>1181</i> copy number and insertion sites correlated with phylogenetic relationships, suggesting that lineage-associated IS<i>1181</i> insertion may contribute to the genomic deletion in <i>S. aureus</i> CC121.</p>

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A subclade-associated genomic deletion encompassing vraDEH confers increased susceptibility to nisin A and bacitracin in Staphylococcus aureus CC121

  • 期刊论文

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  • 发表日期：

    2026年6月19日

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  • Yujin Suzuki,
  • Airi Odawara,
  • Miki Kawada-Matsuo,
  • Junzo Hisatsune,
  • Chika Arai,
  • Saki Nishihama,
  • Hideki Shiba,
  • Souichi Yanamoto,
  • Takemasa Sakaguchi,
  • Motoyuki Sugai,
  • Hitoshi Komatsuzawa

摘要

Antimicrobial peptides (AMPs) play important roles in suppressing bacterial colonization and infection, and several AMPs are used as antimicrobial agents. Conversely, bacteria possess mechanisms that confer resistance to AMPs. We previously identified clinical Staphylococcus aureus isolates lacking the vraDEH genes, which are involved in nisin and bacitracin resistance. All such isolates belonged to clonal complex (CC) 121 and exhibited increased susceptibility to nisin A and bacitracin. The absence of vraDEH was accompanied by the absence of a 35,005-bp genomic region encompassing the biofilm-associated icaRADBC genes and a histidine biosynthesis operon. In a vraDEH-positive CC121 strain, this region was flanked by two IS1181 elements, whereas in vraDEH-negative strains it was replaced by a single IS1181 element, suggesting deletion through recombination between IS elements. Analysis of publicly available genomes revealed that all strains carrying the 35-kb deletion belonged to a single phylogenetic subclade of CC121. The downstream IS1181 insertion was frequently found in CC121 strains, whereas the upstream insertion was only found in this subclade. Across the S. aureus population, IS1181 copy number and insertion sites correlated with phylogenetic relationships, suggesting that lineage-associated IS1181 insertion may contribute to the genomic deletion in S. aureus CC121.