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

Suppression of respiratory growth defect of mutant deficient in mitochondrial phospholipase A1 by overexpression of genes involved in coenzyme Q synthesis in Saccharomyces cerevisiae
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通过过度表达酿酒酵母中参与辅酶 Q 合成的基因来抑制线粒体磷脂酶 A1 缺陷突变体的呼吸生长缺陷

DOI:
10.1080/09168451.2018.1476124
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发表时间:
2018
期刊:
Bioscience, Biotechnology, and Biochemistry
影响因子:
--
通讯作者:
Ryouichi Fukuda
Ryouichi Fukuda
中科院分区:
--
文献类型:
--
作者:
Shiho Morisada;Ikuhisa Nishida;Makoto Kawamukai;Hiroyuki Horiuchi;Ryouichi Fukuda

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DDL1编码一种线粒体磷脂酶A1,参与酿酒酵母线粒体磷脂的酰基链重塑和心磷脂的降解。DDL1的缺失导致呼吸生长缺陷。为了阐明DDL1的生理作用,我们筛选了在过表达时抑制DDL1缺失突变体呼吸生长缺陷的基因。使用多拷贝载体导入参与辅酶Q(CoQ)合成的COQ 8、COQ 9或COQ 5抑制了DDL1缺失突变体的呼吸生长缺陷。相反,使用多拷贝载体导入COQ 8并没有加速TAZ 1或CLD 1缺失突变体的生长,TAZ 1或CLD 1分别编码酰基转移酶或磷脂酶A2,参与心磷脂的重塑。这些结果表明线粒体磷脂酶A1基因和辅酶Q合成相关基因之间存在遗传相互作用。
DDL1encodes a mitochondrial phospholipase A1involved in acyl chain remodeling of mitochondrial phospholipids and degradation of cardiolipin inSaccharomyces cerevisiae. The deletion ofDDL1leads to respiratory growth defects. To elucidate the physiological role ofDDL1, we screened for genes that, when overexpressed, suppress the respiratory growth defect of theDDL1deletion mutant. Introduction ofCOQ8, COQ9, orCOQ5, which are involved in coenzyme Q (CoQ) synthesis, using a multicopy vector suppressed the respiratory growth defect of theDDL1deletion mutant. In contrast, introduction ofCOQ8using a multicopy vector did not accelerate the growth of the deletion mutants ofTAZ1orCLD1, which encode an acyltransferase or phospholipase A2, respectively, involved in the remodeling of cardiolipin. These results suggest genetic interactions between the mitochondrial phospholipase A1gene and the genes involved in CoQ synthesis.
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