核糖体缺陷会在宿主细胞内诱导沙门氏菌丝状的形成
Zhihui Lyu1, Cierra Wilson1, Kalyn Weiss2
1Department of Cell Biology and Molecular Genetics, The University of Maryland, College Park, Maryland, USA.
mBio
|June 30, 2025
概括
核糖体缺陷导致沙门氏菌从杆状转变为宿主细胞内的丝状,改善了在酸性压力下的生存能力. 这种形态变化与胺操作子调节有关,并且可以通过抗生素诱导.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 遗传学 遗传学 是一个
背景情况:
- 细菌面临宿主诱导的压力,促使像形态变化这样的适应机制.
- 核糖体功能对于细菌的生存至关重要,是抗生素的点.
- 核糖体缺陷会影响细菌的应激反应,但其在宿主-病原体相互作用中的作用尚不清楚.
研究的目的:
- 为了研究核糖体缺陷对宿主细胞内的细菌形态的影响.
- 阐明导致沙门氏菌核糖体缺陷引起的形态变化的分子机制.
- 为了确定宿主-病原体相互作用期间的细菌线丝的适应意义.
主要方法:
- 使用了缺少核糖体的沙门氏菌株和宿主巨细胞感染模型.
- 采用基因分析来确定关键的调节基因和途径.
- 结合分子和细胞生物学技术,研究基因表达和细胞形态.
主要成果:
- 缺乏核糖体的沙门氏菌在巨细胞内表现出从杆状到丝状的形态转变.
- 纤维化取决于酸性条件,并与司丁操作子 (his) 的过度表达有关.
- 突变体中HisL领导的缓慢翻译激活了其操作转录,诱导了丝状结构.
结论:
- 核糖体缺陷,无论是由于突变还是抗生素,都会在宿主细胞中触发沙门氏菌线.
- 细菌纤维化作为一种适应性策略,增强在酸性压力下生存.
- 这项研究揭示了细菌形态和适应宿主环境的转化控制.
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