Phenol soluble modulins (PSMs) are responsible for regulating the following: biofilm formation, persister cell formation, pmtR expression, host cell lysis, and anti-bacterial effects. To determine the effect of psm deletion on MRSA, psm deletion mutants, such as Δpsmα, Δpsmβ, and Δpsmαβ, respectively, were studied; these mutants showed increased β-lactam antibiotic resistance to ampicillin and oxacillin. This resistance was shown to be caused by increased N acetylmannosamine kinase (nanK) mRNA expression that regulates persister cell formation, a change in the pattern of phospholipid fatty acids resulting in increased anteiso-C_15:0, and increased membrane hydrophobicity with the deletion of PSMs. When synthetic PSMs were applied to Δpsmα and Δpsmβ mutants, treatment of Δpsmα with PSMα1-4 and Δpsmβ with PSMβ1-2 restored the sensitivity to oxacillin and slightly reduced the biofilm formation. Addition of a single fragment showed that α1, α2, α3, and β2 had an inhibiting effect on biofilms in Δpsmα; however, β1 showed an enhancing effect on biofilms in Δpsmβ. This study demonstrated a possible reason for the increased antibiotic resistance in psm mutants and the effect of PSMs on biofilm formation.

中文翻译：

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耐甲氧西林金黄色葡萄球菌 USA300 Δpsm 突变体的抗生素耐药性增加以及使用合成酚可溶性调节蛋白对 Δpsm 突变体进行的互补研究。

酚溶性调节蛋白 (PSM) 负责调节以下各项：生物膜形成、持久细胞形成、pmtR表达、宿主细胞裂解和抗菌作用。为了确定psm缺失对 MRSA的影响，分别研究了psm缺失突变体，例如Δpsmα、Δpsmβ和Δpsmαβ ；这些突变体显示出对氨苄青霉素和苯唑西林的 β-内酰胺抗生素耐药性增加。这种抗性被证明是由调节持久细胞形成的 N 乙酰甘露糖胺激酶 ( nanK ) mRNA 表达增加引起的，磷脂脂肪酸模式的变化导致反异-C _15:0增加, 并随着 PSM 的删除而增加膜的疏水性。当合成 PSM 应用于Δpsmα和Δpsmβ突变体时，用 PSMα1-4 处理Δpsmα和用PSMβ1-2处理 Δpsmβ 恢复对苯唑西林的敏感性并略微减少生物膜形成。添加单个片段显示α1、α2、α3和β2对Δpsmα中的生物膜具有抑制作用；然而，β1 显示出对Δpsmβ中生物膜的增强作用。这项研究证明了psm突变体中抗生素耐药性增加的可能原因以及 PSM 对生物膜形成的影响。