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酿酒酵母的pel1突变体缺乏心磷脂,并且在编码磷脂酰丝氨酸合酶的CHO1基因被破坏后无法存活。

The pel1 mutant of Saccharomyces cerevisiae is deficient in cardiolipin and does not survive the disruption of the CHO1 gene encoding phosphatidylserine synthase.

作者信息

Janitor M, Obernauerová M, Kohlwein S D, Subík J

机构信息

Comenius University, Department of Microbiology and Virology, Bratislava, Slovak Republic.

出版信息

FEMS Microbiol Lett. 1996 Jun 15;140(1):43-7. doi: 10.1111/j.1574-6968.1996.tb08312.x.

Abstract

Cells of the pel1 mutant of Saccharomyces cerevisiae were found to contain an extremely low content of cardiolipin, a decreased level of phosphatidylcholine and an increased level of phosphatidylinositol. Disruption of the PEL1 gene in cells containing a null mutation in the CHO1 gene was lethal. Despite its putative functional homology with CHO1, the overexpression of the PEL1 gene in the cho1 null mutant did not restore the wild-type properties of the transformed cells and failed to stimulate the incorporation of L-[3-3H]serine into total lipids of the intact yeast cells.

摘要

酿酒酵母pel1突变体的细胞被发现含有极低含量的心磷脂、降低的磷脂酰胆碱水平和升高的磷脂酰肌醇水平。在CHO1基因存在无效突变的细胞中破坏PEL1基因是致死性的。尽管PEL1与CHO1具有假定的功能同源性,但在cho1无效突变体中过表达PEL1基因并不能恢复转化细胞的野生型特性,也无法刺激L-[3-³H]丝氨酸掺入完整酵母细胞的总脂质中。

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