与致病性岛屿的转录诱导域相关的细菌染色质重塑
Mounia Kortebi1, Mickaël Bourge1, Romain Le Bars1
1Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France.
细菌蛋白H-NS可以使病原性基因沉默. 在激活后,H-NS重塑和Hild促进沙门氏菌致病性岛1 (SPI-1) 的表达,改变染色质和定位宿主入侵.
科学领域:
- 微生物学 微生物学
- 细菌遗传学 细菌遗传学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 核相关蛋白H-NS作为一种细菌异原体沉声器.
- H-NS对于沉默沙门氏菌病原性岛屿 (SPI) 至关重要,这对宿主感染至关重要.
- SPI-1的随机表达对于上皮细胞入侵至关重要,但使调控研究复杂化.
研究的目的:
- 研究SPI-1激活对染色体组成,DNA构造,基因表达和亚细胞局部化的影响.
- 描述H-NS占用改造在SPI-1法规中的作用.
- 了解H-NS,Hild和SPI-1激活之间的相互作用.
主要方法:
- 在排序的沙门氏菌种群上的功能基因组学.
- 对染色质组成和DNA构成的分析.
- 基因表达概况和亚细胞局部化研究.
主要成果:
- 沉默的SPI表现出来自H-NS无区域的虚假反意义转录活性.
- SPI-1激活涉及H-NS占用重塑,创建一个新的染色体景观.
- H-NS重塑和调节器Hild促进SPI-1基因转录和转录诱导域的形成.
- SPI-1的激活导致SPI-1在核周边附近的重新定位.
结论:
- 介绍了一种在致病性岛屿激活期间严格调节的染色质重塑的模型.
- 这种改造过程最大限度地降低了与激活病原性岛屿相关的能量成本.
- 在细菌病变发生过程中,H-NS在调节基因表达方面发挥着动态作用.
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