Scholarlink

<p>Methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) is a leading cause of invasive infections, yet the genetic basis of its stress adaptation remains partially understood. This study investigates the role of the conserved membrane-associated gene <i>ytrE</i> in MRSA USA300 pathogenesis. While disruption of <i>ytrE</i> did not affect in vitro growth or biofilm formation, the Δ<i>ytrE</i> mutant exhibited significant attenuation in a murine systemic infection model, characterized by increased host survival and reduced bacterial burdens in major organs. Phenotypic analyses revealed that loss of <i>ytrE</i> leads to compromised membrane integrity, impaired surface-associated motility, and heightened sensitivity to oxidative stress (H<sub>2</sub>O<sub>2</sub>). Furthermore, the mutant showed reduced levels of cell-associated phenol-soluble modulins (PSMs), which may contribute to the impaired colony spreading phenotype. Genetic complementation restored the major altered phenotypes observed in the Δ<i>ytrE</i> mutant. These findings suggest that <i>ytrE</i> contributes to MRSA pathogenic fitness by supporting envelope homeostasis and resistance to oxidative stress. Non-essential factors involved in membrane stability may represent potential targets for future anti-virulence studies.</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

Disruption of ytrE attenuates methicillin-resistant Staphylococcus aureus virulence and compromises membrane integrity and oxidative stress resistance

  • 期刊论文

  • 发表日期：

    2026年8月3日

查看全文
  • Jianhua Liao,
  • Chaodan Shao,
  • Dongli Yu,
  • Yuechun Wang,
  • Xiaoxia Shou

摘要

Methicillin-resistant Staphylococcus aureus (MRSA) is a leading cause of invasive infections, yet the genetic basis of its stress adaptation remains partially understood. This study investigates the role of the conserved membrane-associated gene ytrE in MRSA USA300 pathogenesis. While disruption of ytrE did not affect in vitro growth or biofilm formation, the ΔytrE mutant exhibited significant attenuation in a murine systemic infection model, characterized by increased host survival and reduced bacterial burdens in major organs. Phenotypic analyses revealed that loss of ytrE leads to compromised membrane integrity, impaired surface-associated motility, and heightened sensitivity to oxidative stress (H2O2). Furthermore, the mutant showed reduced levels of cell-associated phenol-soluble modulins (PSMs), which may contribute to the impaired colony spreading phenotype. Genetic complementation restored the major altered phenotypes observed in the ΔytrE mutant. These findings suggest that ytrE contributes to MRSA pathogenic fitness by supporting envelope homeostasis and resistance to oxidative stress. Non-essential factors involved in membrane stability may represent potential targets for future anti-virulence studies.