在Bacillus anthracis中,FapR调节了通过HssRS介导的血稳定
Hualiang Pi1,2,3, Sophia M Carlin1,2, William N Beavers1,2
1Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University, Nashville, TN.
脂肪酸生物合成调节器FapR控制Bacillus anthracis.中的HssRS两个组成系统. 破坏FapR会使HssRS失活,从而影响细菌适应有毒血水平.
科学领域:
- 微生物学 微生物学
- 细菌病原体的产生
- 分子生物学分子生物学
背景情况:
- 炭杆菌 (Bacillus anthracis) 引起炭,并在脊椎动物的血液中壮成长,导致高血暴露.
- 血红素是一种重要的营养素,但过量有毒,需要细菌血红素恒温机制.
- 两个组成的HssRS系统调节了B. anthracis的血毒性,但其调节还没有完全理解.
研究的目的:
- 研究脂肪酸生物合成调节剂FapR在B. anthracis HssRS系统的功能中的作用.
- 阐明FapR影响细菌适应血压的分子机制.
主要方法:
- 在B. anthracis.中fAPR基因的遗传破坏.
- 在野生型和FapR突变菌株中分析HssRS系统活性和血红素稳定.
- 细胞膜完整性和HssS局部化的评估.
主要成果:
- 破坏fapR导致膜刚度增加,阻碍HssRS诱导器的透,并使系统失活.
- 删除fapR破坏了对血红素敏感的胺激酶 (histidine kinase) HssS在细胞膜上的定位.
- 失去FapR功能会减少内源性血红素生物合成,影响细菌适应血红素应激.
结论:
- 在B. anthracis. 中,FapR是HssRS两组系统的关键调节器.
- FapR通过影响膜特性和HssS定位来维持HssRS功能.
- 针对FapR或其下游效应,可以提供针对炭菌的新型抗菌策略.
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