伯克霍尔德里亚伪 BipD调节宿主线粒,以逃避杀戮
Dongqi Nan1, Chenglong Rao1, Zhiheng Tang2
1Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Nature communications
|June 4, 2024
概括
Burkholderia pseudomallei使用BipD蛋白来劫持宿主线粒细胞吸收,这是一个清除受损线粒体的细胞过程. 这种细菌操纵涉及IMMT蛋白的无处不在,有助于病原体的生存.
科学领域:
- 细胞生物学 细胞生物学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 线粒体是维护线粒体健康和功能的关键细胞机制,通过去除受损的线粒体.
- 细胞内细菌病原体往往会发展出策略来操纵宿主细胞过程,以实现它们的生存和复制.
研究的目的:
- 为了研究Burkholderia pseudomallei利用宿主线粒细胞吸收用于细胞内生存的机制.
- 为了确定参与这种操纵的细菌因素和宿主蛋白质.
主要方法:
- 确定了细菌蛋白BipD作为一个关键的效应因子.
- 通过生物化学分析,研究了BipD与宿主蛋白 KLHL9,KLHL13 和 CUL3 之间的相互作用.
- 利用宿主无处不在的分析来识别线粒体基质.
- 进行了ubiquitination测定,并评估了小鼠巨细胞中的线粒细胞诱导.
主要成果:
- BipD与KLHL9/KLHL13/CUL3 E3结合酶复合体相互作用,调解了BipD依赖的线粒体无化.
- 内线粒体膜蛋白IMMT被确定为KLHL9/KLHL13/CUL3复合物的基质.
- 这个复合体在K211的IMMT与K63结合的泛化对于启动线粒是必不可少的.
- 这一过程减少了线粒体的活性氧物种 (ROS) 生产,促进了细菌的生存.
结论:
- Burkholderia pseudomallei采用了一种涉及III型分泌系统蛋白BipD的新机制,以劫持宿主线粒.
- 细菌操纵针对IMMT蛋白进行无处不在,触发线粒并抑制ROS.
- 这项研究揭示了一种独特的细菌策略,利用宿主线粒体质量控制来实现细胞内生存.
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