Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Department of Microbiology and Infectious Disease Center, NHC Key Laboratory of Medical Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Nat Commun. 2024 Jun 4;15(1):4740. doi: 10.1038/s41467-024-48824-x.
Mitophagy is critical for mitochondrial quality control and function to clear damaged mitochondria. Here, we found that Burkholderia pseudomallei maneuvered host mitophagy for its intracellular survival through the type III secretion system needle tip protein BipD. We identified BipD, interacting with BTB-containing proteins KLHL9 and KLHL13 by binding to the Back and Kelch domains, recruited NEDD8 family RING E3 ligase CUL3 in response to B. pseudomallei infection. Although evidently not involved in regulation of infectious diseases, KLHL9/KLHL13/CUL3 E3 ligase complex was essential for BipD-dependent ubiquitination of mitochondria in mouse macrophages. Mechanistically, we discovered the inner mitochondrial membrane IMMT via host ubiquitome profiling as a substrate of KLHL9/KLHL13/CUL3 complex. Notably, K63-linked ubiquitination of IMMT K211 was required for initiating host mitophagy, thereby reducing mitochondrial ROS production. Here, we show a unique mechanism used by bacterial pathogens that hijacks host mitophagy for their survival.
自噬对于线粒体的质量控制和功能清除受损的线粒体至关重要。在这里,我们发现伯克霍尔德氏菌通过 III 型分泌系统针状蛋白 BipD 操纵宿主自噬以实现其细胞内生存。我们发现 BipD 通过与 Back 和 Kelch 结构域结合,与含有 BTB 的蛋白质 KLHL9 和 KLHL13 相互作用,在受到伯克霍尔德氏菌感染时募集 NEDD8 家族 RING E3 连接酶 CUL3。尽管显然不参与传染病的调节,但 KLHL9/KLHL13/CUL3 E3 连接酶复合物对于 BipD 依赖性鼠巨噬细胞中线粒体的泛素化至关重要。在机制上,我们通过宿主泛素组谱发现了作为 KLHL9/KLHL13/CUL3 复合物底物的内线粒体膜 IMMT。值得注意的是,IMMT K211 的 K63 连接泛素化对于启动宿主自噬从而减少线粒体 ROS 产生是必需的。在这里,我们展示了细菌病原体利用宿主自噬进行生存的独特机制。