该CarSR双组件系统直接控制radD表达作为一个全球调节器,感知Fusobacterium核中的细菌凝聚
bioRxiv : the preprint server for biology
|December 23, 2024
概括
Fusobacterium nucleatum使用CarSR两组系统来调节粘附和营养利用. 与其他细菌的凝聚作用为信号,影响基因表达和口腔生物膜的形成.
科学领域:
- 微生物学 微生物学
- 细菌遗传学 细菌遗传学
- 口腔微生物组是口腔的微生物组.
背景情况:
- 核菌 (Fusobacterium nucleatum) 是生物膜中的一个关键的口腔细菌,它弥合了早期和晚期殖民者.
- 它与其他细菌聚合的能力对于牙斑形成至关重要.
- 对于这些相互作用的感知和响应机制尚不清楚.
研究的目的:
- 调查CarSR双组件系统在F. nucleatum.中调节RadD粘附中的作用.
- 为了识别更广泛的CarR规则和CarSR系统感知到的信号.
- 阐明口腔生物膜中细菌传播和适应的机制.
主要方法:
- 染色体免疫沉测序 (ChIP-seq) 用于识别CarR结合部位.
- 电泳运动转移测试 (EMSA),突变发生和DNase I足迹测试,以验证CarR-DNA相互作用.
- RNA-Seq分析以揭示基因表达变化.
主要成果:
- ChIP-seq确定了~161个Carr丰富的位置和一个17bp的共识动机.
- 卡尔直接与radABCD操作子的促进子结合,调节RadD表达.
- 卡尔R还调节参与果糖和氨基酸利用的基因,作为全球调节器.
- 凝聚增强radD表达,这取决于CarS组件,这表明凝聚是一种感知信号.
结论:
- 在F. nucleatum中,CarSR TCS是全球调节者,控制粘附和新陈代谢.
- 凝聚作为一个由CarSR系统感知到的环境信号,调节细菌相互作用.
- 这项研究揭示了F. nucleatum在口腔生物膜动态中的适应和作用的新机制.
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