Department of Life Science, Rikkyo University, Tokyo, Japan.
Department of Bioscience, Graduate School of Agriculture, Ehime University, Japan.
FEBS Lett. 2018 Jan;592(2):209-218. doi: 10.1002/1873-3468.12948. Epub 2017 Dec 27.
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.
线粒体管状结构通过膜融合和裂变之间的平衡来维持，这种平衡受多种因素的调节，包括 Drp1 和线粒体融合蛋白/ fzo-1。在这里，我们报告了心磷脂（CL）合酶在调节线粒体形态中的作用。CL 合酶的敲低诱导线虫和人类细胞中线粒体的伸长。线虫心磷脂合酶和 drp-1 或 fzo-1 的敲低表明，CL 合酶的敲低会减少线粒体的分裂。对人类 CL 合酶敲低细胞的质谱分析显示 CL 的含量减少，而 CL 的前体磷脂酰甘油的积累。其他参与 CL 合成的基因的敲低并不影响线粒体的形态。因此，线粒体的伸长可能是由于磷脂酰甘油的积累，而不是 CL 的减少。
