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Inactivation of cardiolipin synthase triggers changes in mitochondrial morphology
Author(s) -
Matsumura Ayaka,
Higuchi Jun,
Watanabe Yasunori,
Kato Masahiro,
Aoki Keigo,
Akabane Shiori,
Endo Toshiya,
Oka Toshihiko
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12948
Subject(s) - cardiolipin , atp synthase , phosphatidylglycerol , microbiology and biotechnology , mitochondrion , gene knockdown , inner mitochondrial membrane , biology , mitochondrial fusion , chemistry , biochemistry , mitochondrial dna , gene , membrane , phospholipid , phosphatidylcholine
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.