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

<i>DDL1</i> encodes a mitochondrial phospholipase A₁ involved in acyl chain remodeling of mitochondrial phospholipids and degradation of cardiolipin in <i>Saccharomyces cerevisiae</i>. The deletion of <i>DDL1</i> leads to respiratory growth defects. To elucidate the physiological role of <i>DDL1</i>, we screened for genes that, when overexpressed, suppress the respiratory growth defect of the <i>DDL1</i> deletion mutant. Introduction of <i>COQ8, COQ9</i>, or <i>COQ5</i>, which are involved in coenzyme Q (CoQ) synthesis, using a multicopy vector suppressed the respiratory growth defect of the <i>DDL1</i> deletion mutant. In contrast, introduction of <i>COQ8</i> using a multicopy vector did not accelerate the growth of the deletion mutants of <i>TAZ1</i> or <i>CLD1</i>, 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. <b>Abbreviations</b>: 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 <i>DDL1</i> encoding a mitochondrial phospholipase A₁ and genes involved in coenzyme Q synthesis.