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<p><i>Staphylococcus aureus</i> is capable of colonizing diverse environments and forming biofilms. In this study, we found that the knockout of NO synthase (NOS) impaired biofilm integrity, resulting in weakened biofilms. We found the deletion of the <i>nos</i> reduced intracellular NO levels, which subsequently altered the S-nitrosylation modification levels of the proteome. This alteration was particularly pronounced in the S-nitrosylation modification of the cysteine residue at position 12 of the MgrA. This modification reduced the binding affinity of MgrA to the promoter of the acetyltransferase gene (<i>icaA</i>), resulting in reduced levels of poly-N-acetyl-β-(1–6)-glucosamine (PIA), a key component of biofilms formed by <i>S. aureus</i>, thereby further weakening biofilm formation. Consequently, we conclude that NOS in <i>S. aureus</i> S-nitrosylates the MgrA through the synthesis of endogenous NO. This process strengthens the interaction between MgrA and the <i>icaA</i> promoter (P<sub><i>icaA</i></sub>), thereby enhancing the synthesis of major polysaccharides in biofilms and promoting biofilm formation.</p>

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The role of nitric oxide synthase in biofilm formation by Staphylococcus aureus

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月18日

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  • Yi Huang,
  • Yu Cheng,
  • Yingying Shi,
  • Xiaoqiong Wang,
  • Samira Khodi Aghmiuni,
  • Ayesha Serwat,
  • Zhengliang Zhang,
  • Xueqin Shu,
  • Baolin Sun

摘要

Staphylococcus aureus is capable of colonizing diverse environments and forming biofilms. In this study, we found that the knockout of NO synthase (NOS) impaired biofilm integrity, resulting in weakened biofilms. We found the deletion of the nos reduced intracellular NO levels, which subsequently altered the S-nitrosylation modification levels of the proteome. This alteration was particularly pronounced in the S-nitrosylation modification of the cysteine residue at position 12 of the MgrA. This modification reduced the binding affinity of MgrA to the promoter of the acetyltransferase gene (icaA), resulting in reduced levels of poly-N-acetyl-β-(1–6)-glucosamine (PIA), a key component of biofilms formed by S. aureus, thereby further weakening biofilm formation. Consequently, we conclude that NOS in S. aureus S-nitrosylates the MgrA through the synthesis of endogenous NO. This process strengthens the interaction between MgrA and the icaA promoter (PicaA), thereby enhancing the synthesis of major polysaccharides in biofilms and promoting biofilm formation.