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首页> 外文期刊>Infection and immunity >Modulation of Cell Wall Structure and Antimicrobial Susceptibility by a Staphylococcus aureus Eukaryote-Like Serine/Threonine Kinase and Phosphatase
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Modulation of Cell Wall Structure and Antimicrobial Susceptibility by a Staphylococcus aureus Eukaryote-Like Serine/Threonine Kinase and Phosphatase

机译：金黄色葡萄球菌真核生物丝氨酸/苏氨酸激酶和磷酸酶对细胞壁结构和抗菌药敏感性的调节

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It is well established that prokaryotes and eukaryotes alike utilize phosphotransfer to regulate cellular functions. One method by which this occurs is via eukaryote-like serine/threonine kinase (ESTK)- and phosphatase (ESTP)-regulated pathways. The role of these enzymes in Staphylococcus aureus has not yet been examined. This resilient organism is a common cause of hospital-acquired and community-associated infections, infecting immunocompromised and immunocompetent hosts alike. In this study, we have characterized a major functional ESTK (STK) and ESTP (STP) in S. aureus and found them to be critical modulators of cell wall structure and susceptibility to cell wall-acting β-lactam antibiotics. By utilizing gene knockout strategies, we created S. aureus N315 mutants lacking STP and/or STK. The strain lacking both STP and STK displayed notable cell division defects, including multiple and incomplete septa, bulging, and irregular cell size, as observed by transmission electron microscopy. Mutants lacking STP alone displayed thickened cell walls and increased resistance to the peptidoglycan-targeting glycylglycine endopeptidase lysostaphin, compared to the wild type. Additionally, mutant strains lacking STK or both STK and STP displayed increased sensitivity to cell wall-acting cephalosporin and carbapenem antibiotics. Together, these results indicate that S. aureus STK- and STP-mediated reversible phosphorylation reactions play a critical role in proper cell wall architecture, and thus the modulation of antimicrobial resistance, in S. aureus.
机译：众所周知，原核生物和真核生物都利用磷酸转移来调节细胞功能。发生这种情况的一种方法是通过真核生物样丝氨酸/苏氨酸激酶（ESTK）和磷酸酶（ESTP）调控的途径。这些酶在金黄色葡萄球菌中的作用尚未得到研究。这种有弹性的生物体是医院获得性感染和社区相关性感染的常见原因，会感染免疫功能低下和具有免疫能力的宿主。在这项研究中，我们表征了 S中的主要功能性ESTK（STK）和ESTP（STP）。并发现它们是细胞壁结构和对细胞壁作用β-内酰胺抗生素敏感性的关键调节剂。通过利用基因敲除策略，我们创建了 S。缺少STP和/或STK的金黄色葡萄球菌N315突变体。缺乏STP和STK的菌株显示出明显的细胞分裂缺陷，包括多个和不完整的隔片，膨出和不规则的细胞大小，如通过透射电子显微镜观察到的。与野生型相比，仅缺乏STP的突变体显示出细胞壁增厚，并且对靶向肽聚糖的甘氨酰甘氨酸内肽酶溶葡萄球菌素的抵抗力增强。此外，缺乏STK或STK和STP都缺乏的突变株显示出对细胞壁作用头孢菌素和碳青霉烯类抗生素的敏感性增加。这些结果加在一起表明 S。金黄色葡萄球菌的STK和STP介导的可逆磷酸化反应在正确的细胞壁结构中起着至关重要的作用，从而在 S中调节抗菌素的耐药性。金黄色。

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