Inactivation of cardiolipin synthase triggers changes in mitochondrial morphology
Inactivation of cardiolipin synthase triggers changes in mitochondrial morphology
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DOI：
10.1002/1873-3468.12948
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发表时间：
2018-01-01
期刊：
影响因子：
3.5
通讯作者：
Oka, Toshihiko
中科院分区：
文献类型：
--
作者：
Matsumura, Ayaka;Higuchi, Jun;Oka, Toshihiko
线粒体管状结构通过膜融合和裂变之间的平衡来维持，该平衡受到多种因素的调节，包括 Drp1 和 mitofusin/fzo-1。在这里，我们报告心磷脂（CL）合酶在线粒体形态调节中的作用。线虫和人类细胞中 CL 合酶的敲低诱导线粒体伸长。线虫心磷脂合酶和 drp-1 或 fzo-1 的敲低表明敲低 CL 合酶会减少线粒体分裂。对人 CL 合酶敲低细胞的质谱分析显示 CL 量减少，并且 CL 前体磷脂酰甘油积累。敲低参与 CL 合成的其他基因并不影响线粒体形态。因此，线粒体伸长可能是由于磷脂酰甘油的积累而不是 CL 的减少所致。
Mitochondrial tubular structures are maintained by a balance between membrane fusion and fission that is regulated by various factors, including Drp1 and mitofusin/fzo-1. Here we report the role of cardiolipin (CL) synthase in the regulation of mitochondrial morphology. Knockdown of CL synthase induced mitochondrial elongation in nematode and human cells. Knockdown of both nematode cardiolipin synthase and drp-1 or fzo-1 suggested that knocking down CL synthase decreases mitochondrial division. Mass spectrometric analysis of human CL synthase-knocked down cells revealed a decreased amount of CL and an accumulation of phosphatidylglycerol, a CL precursor. Knockdown of other genes involved in CL synthesis did not influence mitochondrial morphology. Thus, mitochondrial elongation may result from the accumulation of phosphatidylglycerol rather than decreased CL.