心磷脂
细胞生物学
线粒体
线粒体融合
线粒体内膜
DNAJA3公司
线粒体载体
ATP-ADP转位酶
生物
阻抑素
线粒体基质
线粒体凋亡诱导通道
胞浆
化学
线粒体DNA
生物化学
细菌外膜
磷脂
基因
膜
酶
大肠杆菌
作者
Svetlana Konovalova,Rubén Torregrosa‐Muñumer,Pooja Manjunath,Sundar Baral,Xiaonan Liu,Minna Holopainen,Jouni Kvist,Jayasimman Rajendran,Yang Yang,Markku Varjosalo,Reijo Käkelä,Pentti Somerharju,Henna Tyynismaa
标识
DOI:10.1101/2021.01.03.424667
摘要
ABSTRACT Cardiolipin (CL) is an essential phospholipid for mitochondrial structure and function. Here we present a small mitochondrial protein, NERCLIN, as a negative regulator of CL homeostasis and mitochondrial ultrastructure. Primate-specific NERCLIN is expressed ubiquitously from GRPEL2 locus on a tightly regulated low level, but induced by heat stress. NERCLIN overexpression severely disrupts mitochondrial cristae structure and induces mitochondrial fragmentation. Proximity labeling suggested interactions of NERCLIN with CL synthesis and prohibitin complexes on the matrix side of the inner mitochondrial membrane. Lipid analysis indicated that NERCLIN regulates mitochondrial CL content. The regulation may occur directly through interaction with PTPMT1, a proximal partner on the CL synthesis pathway, as its product phosphatidylglycerol was also reduced by NERCLIN. We propose that NERCLIN contributes to stress-induced adaptation of mitochondrial dynamics and turnover by regulating the mitochondrial CL content. Our findings add NERCLIN to the group of recently identified small mitochondrial proteins with important regulatory functions.
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