FMP30 is required for the maintenance of a normal cardiolipin level and mitochondrial morphology in the absence of mitochondrial phosphatidylethanolamine synthesis

Takuya Kuroda, Motohiro Tani, Akira Moriguchi, Sho Tokunaga, Takahito Higuchi, Sakae Kitada, Osamu Kuge

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)

Abstract

Mitochondria of the yeast Saccharomyces cerevisiae contain enzymes Crd1p and Psd1p, which synthesize cardiolipin (CL) and phosphatidylethanolamine respectively. A previous study indicated that crd1Δ is synthetically lethal with psd1Δ. In this study, to identify novel genes involved in CL metabolism, we searched for genes that genetically interact with Psd1p, and found that deletion of FMP30 encoding a mitochondrial inner membrane protein results in a synthetic growth defect with psd1Δ. Although fmp30Δ cells grew normally and exhibited a slightly decreased CL level, fmp30Δpsd1Δ cells exhibited a severe growth defect and an about 20-fold reduction in the CL level, as compared with the wild-type control. We found also that deletion of FMP30 caused a defect in mitochondrial morphology. Furthermore, FMP30 genetically interacted with seven mitochondrial morphology genes. These results indicated that Fmp30p is involved in the maintenance of mitochondrial morphology and required for the accumulation of a normal level of CL in the absence of mitochondrial phosphatidylethanolamine synthesis.

Original languageEnglish
Pages (from-to)248-265
Number of pages18
JournalMolecular Microbiology
Volume80
Issue number1
DOIs
Publication statusPublished - Apr 1 2011

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Molecular Biology

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