体编码的甲基转移酶驱动了社区获得的抗甲素的金黄色葡萄球菌的适应
Robert J Ulrich1, Magdalena Podkowik1,2, Rebecca Tierce3
1Department of Medicine, NYU Grossman School of Medicine, New York, NY, USA.
bioRxiv : the preprint server for biology
|April 25, 2024
概括
黄金葡萄球菌毒性的一种新机制涉及表观遗传调节. 一种菌体编码的酶,pamA,通过调节纤维素结合蛋白A (fnbA) 的上升来增加皮肤的尺寸,促进生物膜的形成.
科学领域:
- 微生物学 微生物学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 美国300种社区获得的抗甲素金黄色葡萄球菌 (CA-MRSA) 已发展出变种.
- 菌体的获取,特别是马赛克 Φ11 (mΦ11),与CA-MRSA皮肤感染中的毒性增加有关.
研究的目的:
- 阐明 mΦ11 孕原在皮肤感染中增强 CA-MRSA 毒性的机制.
- 为了确定涉及mΦ11介导毒性的特定基因和途径.
主要方法:
- 研究了mΦ11编码的腺因甲基转移酶 (pamA) 在毒性中的作用.
- 评估了pamA对纤维素结合蛋白A (fnbA) 表达的影响.
- 研究了pamA和fnbA无活化的对腹大小和体内炎症的影响.
- 分析了pamA在促进皮肤腹内生物膜形成中的作用.
主要成果:
- 的尺寸和皮肤炎症与pamA的DNA甲基酶活性相关.
- pamA显著增加了fnbA的表达.
- 禁用fnbA取消了pamA对毒性的影响,确认fnbA是pamA特有的毒性因子.
- 通过FnBPA的介导,pamA被证明可以促进皮肤的体内生物膜形成.
结论:
- 菌体mΦ11通过通过pamA进行表观遗传修饰来调节金黄色葡萄球菌的毒性.
- 在皮肤中,pamA通过调节fnbA来增强毒性,从而促进皮肤中生物膜的形成.
- 这项研究揭示了通过表观遗传控制葡萄球菌基因表达的菌媒介病毒性调节的新机制.
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