Atkinson K, Fogel S, Henry S A
J Biol Chem. 1980 Jul 25;255(14):6653-61.
Phospholipid biosynthesis in a mutant of Saccharomyces cerevisiae (cho1) which lacks phosphatidylserine (Atkinson, K. D., Jensen, B., Storm, E., Kolat, A. I., Henry, S. A. & Fogel, S. (1980) J. Bacteriol. 141, 558-564) has been examined. The ability of cells of this strain to synthesize phosphatidylserine in vitro in a cell-free system is reduced at least 10-fold, whereas other phospholipid-synthesizing activities are present at normal or slightly elevated levels. While all phospholipid biosynthetic activities, except phosphatidylserine synthesis, can be demonstrated in vitro in the cho1 mutant, the entire pattern of phospholipid synthesis, accumulation, and turnover in vivo is distorted. Phosphatidylinositol synthesis is elevated, as is phosphatidylcholine synthesis. In addition, the turnover of phosphatidylcholine is more rapid in the cho1 mutant. The cho1 mutant appears to use almost exclusively the alternative pathway described by Kennedy and Weiss (1956) J. Biol. Chem. 222, 193-214) for the production of phosphatidylethanolamine and phosphatidylcholine, bypassing phosphatidylserine as an intermediate.
对酿酒酵母(cho1)的一个缺乏磷脂酰丝氨酸的突变体中的磷脂生物合成进行了研究(阿特金森,K.D.,詹森,B.,斯托姆,E.,科拉特,A.I.,亨利,S.A.和福格尔,S.(1980年)《细菌学杂志》141,558 - 564)。该菌株细胞在无细胞体系中体外合成磷脂酰丝氨酸的能力至少降低了10倍,而其他磷脂合成活性则处于正常或略高的水平。虽然除了磷脂酰丝氨酸合成外,cho1突变体中的所有磷脂生物合成活性都能在体外得到证明,但体内磷脂合成、积累和周转的整个模式都被扭曲了。磷脂酰肌醇合成增加,磷脂酰胆碱合成也增加。此外,cho1突变体中磷脂酰胆碱的周转更快。cho1突变体似乎几乎完全使用肯尼迪和韦斯(1956年)《生物化学杂志》222,193 - 214)描述的替代途径来产生磷脂酰乙醇胺和磷脂酰胆碱,绕过磷脂酰丝氨酸作为中间产物。