Impaired respiration elicits SrrAB-dependent programmed cell lysis and biofilm formation in Staphylococcus aureus
Impaired respiration elicits SrrAB-dependent programmed cell lysis and biofilm formation in Staphylococcus aureus
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DOI：
10.7554/elife.23845
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发表时间：
2017-02-21
期刊：
影响因子：
7.7
通讯作者：
Boyd, Jeffrey M.
中科院分区：
文献类型：
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作者：
Mashruwala, Ameya A.;van de Guchte, Adriana;Boyd, Jeffrey M.
生物膜是附着在表面或彼此附着的微生物群落。生物膜相关细胞是复发性金黄色葡萄球菌感染的病原体。受感染的人体组织是缺氧的。S.金黄色葡萄球菌增加生物膜的形成，以响应缺氧，但如何发生这是未知的。在目前的研究中，我们报告说，氧气影响生物膜的形成，其能力作为终端电子受体的细胞呼吸。呼吸过程的遗传、生理或化学抑制引起生物膜形成增加。受损的呼吸导致增加细胞溶解通过两个过程的分歧调节：增加的AtIA胞壁酶水解酶的表达和壁磷壁酸的表达减少。细胞质DNA的AItA依赖性释放有助于增加生物膜形成。此外，细胞裂解和生物膜形成由SrrAB双组分调节系统控制。提供的数据支持一个模型，其中SrrAB依赖性生物膜形成响应于还原的甲基萘醌的积累而发生。
Biofilms are communities of microorganisms attached to a surface or each other. Biofilm-associated cells are the etiologic agents of recurrent Staphylococcus aureus infections. Infected human tissues are hypoxic or anoxic. S. aureus increases biofilm formation in response to hypoxia, but how this occurs is unknown. In the current study we report that oxygen influences biofilm formation in its capacity as a terminal electron acceptor for cellular respiration. Genetic, physiological, or chemical inhibition of respiratory processes elicited increased biofilm formation. Impaired respiration led to increased cell lysis via divergent regulation of two processes: increased expression of the AtIA murein hydrolase and decreased expression of wall-teichoic acids. The AItA-dependent release of cytosolic DNA contributed to increased biofilm formation. Further, cell lysis and biofilm formation were governed by the SrrAB two-component regulatory system. Data presented support a model wherein SrrAB-dependent biofilm formation occurs in response to the accumulation of reduced menaquinone.