The Q225P Mutation in SigB Promotes Membrane Vesicle Formation in Staphylococcus aureus.
The Q225P Mutation in SigB Promotes Membrane Vesicle Formation in Staphylococcus aureus.
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DOI：
10.1007/s00284-022-02772-1
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发表时间：
2022-02-01
影响因子：
2.6
通讯作者：
Zhou R
中科院分区：
文献类型：
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作者：
Qiao L;Yang Y;Zhu K;Rao Y;Li G;Rao X;Li M;Zhou R
革兰氏阳性菌和革兰氏阴性菌都释放纳米尺寸的脂质双层颗粒，称为膜囊泡（MV），进入外部环境。尽管MV在细菌生理学和致病机理中发挥多种作用，但革兰氏阳性微生物如金黄色葡萄球菌中MV形成的潜在机制仍然不清楚。细菌MV产生可响应于应激条件而被诱导，并且替代σ因子B（SigB）在革兰氏阳性细菌中作为应激反应的中心调节物起作用。在先前的研究中，我们证明了S.金黄色葡萄球菌促进生物膜形成。在这里，我们报告说，SigB（Q225 P）突变也增加了MV生产在这个重要的病原体。LacZ报告基因分析和电泳迁移率变动分析表明，Q225 P取代减少了SigB与热单核酸酶基因（nuc）启动子区的结合，导致Nuc表达显著减少。nuc的缺失显著增强了S.金黄色葡萄球菌MV的产生，可能是由于核酸的积累。这些结果不仅对理解MV在S.金黄色葡萄球菌，但也可用于发展的S.基于aureus MV的MV应用平台。在线版本包含补充材料，可通过10.1007/s 00284 -022-02772-1获得。
Both Gram-positive and Gram-negative bacteria release nano-sized lipid bilayered particles, known as membrane vesicles (MVs), into external environments. Although MVs play a variety of roles in bacterial physiology and pathogenesis, the mechanisms underlying MV formation in Gram-positive microorganisms such as Staphylococcus aureus remain obscure. Bacterial MV production can be induced in response to stress conditions, and the alternative sigma factor B (SigB) functions as a central regulator of the stress response in Gram-positive bacteria. In a previous study, we demonstrated that the SigB(Q225P) substitution mutation in S. aureus promotes biofilm formation. Here, we report that the SigB(Q225P) mutation also increases MV production in this important pathogen. LacZ reporter assays and electrophoretic mobility shift assays showed that the Q225P substitution reduces SigB binding to the promoter region of the thermonuclease gene (nuc), resulting in a significant reduction in Nuc expression. Deletion of nuc markedly enhances S. aureus MV generation, possibly due to the accumulation of nucleic acids. These results are not only important for understanding MV biogenesis in S. aureus, but also useful for the development of a S. aureus MV-based platform for MV application. The online version contains supplementary material available at 10.1007/s00284-022-02772-1.
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