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Suppression of respiratory growth defect of mutant deficient in mitochondrial phospholipase A1 by overexpression of genes involved in coenzyme Q synthesis in Saccharomyces cerevisiae

posted on 28.05.2018, 08:35 authored by Shiho Morisada, Ikuhisa Nishida, Makoto Kawamukai, Hiroyuki Horiuchi, Ryouichi Fukuda

DDL1 encodes a mitochondrial phospholipase A1 involved in acyl chain remodeling of mitochondrial phospholipids and degradation of cardiolipin in Saccharomyces cerevisiae. The deletion of DDL1 leads to respiratory growth defects. To elucidate the physiological role of DDL1, we screened for genes that, when overexpressed, suppress the respiratory growth defect of the DDL1 deletion mutant. Introduction of COQ8, COQ9, or COQ5, which are involved in coenzyme Q (CoQ) synthesis, using a multicopy vector suppressed the respiratory growth defect of the DDL1 deletion mutant. In contrast, introduction of COQ8 using a multicopy vector did not accelerate the growth of the deletion mutants of TAZ1 or CLD1, which encode an acyltransferase or phospholipase A2, respectively, involved in the remodeling of cardiolipin. These results suggest genetic interactions between the mitochondrial phospholipase A1 gene and the genes involved in CoQ synthesis.

Abbreviations: CoQ: coenzyme Q; CL: cardiolipin; ORF: open reading frame; PA: phosphatidic acid; PC: phosphatidylcholine; PE: phosphatidylethanolamine; PG: phosphatidylglycerol; PLA1: phospholipase A1; iPLA1: intracellular PLA1; PLA2: phospholipase A2

Genetic interaction between DDL1 encoding a mitochondrial phospholipase A1 and genes involved in coenzyme Q synthesis.


This work was partly supported by Japan Society for the Promotion of Science [grant numbers 17K07710, 23580104]