Golgi-derived PI(4)P-containing vesicles drive late steps of mitochondrial division

被引：172

作者：

Nagashima, Shun ^{[1
]}

Tabara, Luis-Carlos ^{[1
]}

Tilokani, Lisa ^{[1
]}

Paupe, Vincent ^{[1
]}

Anand, Hanish ^{[1
]}

Pogson, Joe H. ^{[2
]}

Zunino, Rodolfo ^{[2
]}

McBride, Heidi M. ^{[2
]}

Prudent, Julien ^{[1
]}

机构：

[1] Univ Cambridge, Med Res Council Mitochondrial Biol Unit, Cambridge Biomed Campus, Cambridge CB2 0XY, England

[2] McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ H3B 2B4, Canada

来源：

SCIENCE | 2020年 / 367卷 / 6484期

基金：

英国惠康基金; 欧盟地平线“2020”; 英国医学研究理事会; 加拿大健康研究院;

关键词：

FISSION; ACTIN; PROTEINS; DRP1; PEROXISOMES; MORPHOLOGY; DYNAMICS; PLATFORM; MAPL; BETA;

D O I：

10.1126/science.aax6089

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：1366 / +

页数：43

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