细胞内细菌劫持了MICOS复杂子单元Mic60,以操纵线粒体动力学并促进细菌病原性
Changyong Cheng1, Mianmian Chen1, Jing Sun1
1Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Zhejiang Provincial Engineering Research Center for Animal Health Diagnostics & Advanced Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China-Australia Joint Laboratory for Animal Health Big Data Analytics, College of Veterinary Medicine of Zhejiang A&F University, 666 Wusu Street, Lin'an District, Hangzhou, Zhejiang Province, 311300, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|October 21, 2024
概括
李斯特菌通过listeriolysin O (LLO) 和Mic60操纵宿主线粒体,导致裂变并增强细菌感染. 这种相互作用会影响线粒体功能和细菌病原性.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 病变的发生和发病.
背景情况:
- 主体线粒体的动态 (裂变/融合) 对细胞过程至关重要.
- 细胞内细菌,如Listeria monocytogenes,经常利用宿主细胞机械生存和复制.
- 线粒体功能障碍越来越被认为是传染病的一个因素.
研究的目的:
- 阐明Listeria monocytogenes操纵宿主线粒体动态的分子机制.
- 为了确定参与这种相互作用的特定细菌因素和宿主蛋白质.
- 了解这种操纵如何促进细菌病原性.
主要方法:
- 研究了Listeria monocytogenes病毒性因子listeriolysin O (LLO) 的作用.
- 使用生物化学分析来研究LLO和Mic60之间的相互作用,这是MICOS复合物的组成部分.
- 分析了LLO-Mic60相互作用对线粒体形态,膜潜力,ROS产生和F-actin尾巴形成的影响.
主要成果:
- L. monocytogenes通过LLO与Mic60的相互作用触发了短暂的线粒体裂变.
- 一个特定的残留物,LLO中的Phe251,对于Mic60结合,线粒体碎片化和细菌致病性至关重要.
- Mic60影响L. monocytogenes招募的F-actin尾巴,其表达受到感染的影响,改变线粒体功能.
结论:
- 通过LLO-Mic60相互作用,L. monocytogenes通过LLO-Mic60相互作用劫持宿主线粒体动态,以促进感染.
- 这种机制涉及对线粒体形态,膜潜力,ROS和F-actin动态的调节.
- 了解这种宿主-病原体相互作用为新的抗菌策略提供了潜力.
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