期刊
SCIENCE
卷 367, 期 6484, 页码 1366-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax6089
关键词
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资金
- Canadian Institutes of Health Research Operating Grants Program (CIHR) [68833]
- Medical Research Council (MRC) [MC_UU_00015/7, RG89175]
- Isaac Newton Trust [RG89529]
- Wellcome Trust Institutional Strategic Support Fund [RG89305]
- Daiichi Sankyo Foundation of Life Science
- Ramon Areces postdoctoral fellowships
- MRC
- European Union's Horizon 2020 research and innovation program [MITODYN-749926]
- MRC [MC_UU_00015/7] Funding Source: UKRI
Mitochondrial plasticity is a key regulator of cell fate decisions. Mitochondrial division involves Dynamin-related protein-1 (Drp1) oligomerization, which constricts membranes at endoplasmic reticulum (ER) contact sites. The mechanisms driving the final steps of mitochondrial division are still unclear. Here, we found that microdomains of phosphatidylinositol 4-phosphate [PI(4)P] on trans-Golgi network (TGN) vesicles were recruited to mitochondria-ER contact sites and could drive mitochondrial division downstream of Drp1. The loss of the small guanosine triphosphatase ADP-ribosylation factor 1 (Arf1) or its effector, phosphatidylinositol 4-kinase III beta [PI(4)KIII beta], in different mammalian cell lines prevented PI(4)P generation and led to a hyperfused and branched mitochondrial network marked with extended mitochondrial constriction sites. Thus, recruitment of TGN-PI(4)P-containing vesicles at mitochondria-ER contact sites may trigger final events leading to mitochondrial scission.
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