细菌硫酸二氧化酶中的自我-S-硫化介导着硫酸硫醇排毒
bioRxiv : the preprint server for biology
|February 27, 2026
概括
硫化二氧化基酶 (PDO) 能够防止硫化中毒. 黄金葡萄球菌 (Staphylococcus aureus CstB) 使用自S化将反应性硫种转化为硫酸硫酸盐,防止毒性.
科学领域:
- 生物化学 生物化学
- 酶学 是一种酶学.
- 微生物学 微生物学
背景情况:
- 二氧化原酶 (PDO) 是关键的非血红素Fe (II) 酶,可以防止硫化 (H2S) 的毒性.
- 细菌的PDO,如金黄色葡萄球菌 (Staphylococcus aureus CstB),通常具有化硫转移酶 (罗丹) 模块,与人类的PDO不同.
- 虽然正规的PDO产量是硫酸盐,但CstB通过一种未知的机制产生硫酸盐.
研究的目的:
- 阐明Staphylococcus aureus CstB将反应性硫种转化为硫酸硫酸盐的机制.
- 研究CstB的催化活性中Cys-Gly基因和罗丹基域的作用.
- 了解CstB如何防止反应性硫物种对细胞产生毒性.
主要方法:
- 六个S. aureus CstB结构的X射线晶体学.
- 生物化学测定以评估酶活性 (O2消耗) 与位点定向突变发生 (C201A,C408A).
- 对自硫化和硫转移途径的分析.
主要成果:
- 六个晶体结构揭示了一个Cys-Gly (C201-G202) 循环,模仿Fe (II) 活性位点上的谷.
- 在C201.1,CstB经历了Fe (II) 和O2依赖的自S硫化.
- 硫被转移到 rhodanese 域中的 C408,产生硫酸盐作为唯一的产物;C201A 和 C408A 突变是不活跃的.
结论:
- CstB使用一种独特的自我-S-硫化机制,涉及C201和C408,以排毒活性硫种.
- 这个过程产生硫酸硫酸盐,防止硫酸盐释放和细胞损伤.
- 自硫化使得S. aureus能够利用活性硫种,同时减轻毒性.
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