Membrane mutants: a yeast mutant with a lesion in phosphatidylserine biosynthesis.
Membrane mutants: a yeast mutant with a lesion in phosphatidylserine biosynthesis.
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膜突变体：磷脂酰丝氨酸生物合成受损的酵母突变体。
DOI：
10.1111/j.1432-1033.1980.tb04965.x
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Vlasta KOVÁČvÁ
中科院分区：
文献类型：
--
作者：
Ladistav Kováč;Iveta Gbelská;V. Poliachová;Julius Subik;Vlasta KOVÁČvÁ
研究了一株酿酒酵母胆碱核单基因突变体。低浓度的二甲基乙醇胺、单甲基乙醇胺或乙醇胺可以替代胆碱作为合成培养基的生长补充物。dl -丝氨酸也支持生长，但只有在高浓度下：在摩尔基础上，它的效果大约比胆碱低一百倍。当在未添加的培养基中培养时，突变细胞很快停止生长。生长受阻的细胞所含的磷脂酰乙醇胺不到野生型细胞的五分之一，而且只有微量的磷脂酰丝氨酸。两种磷脂的相对含量通过在其他补充物胆碱的存在下培养突变细胞而提高，但仍低于野生型细胞。缺乏磷脂酰乙醇胺和磷脂酰丝氨酸的突变体细胞在交配中与其他细胞融合的能力大大降低，其原生质体对低压裂解的抵抗力增强。突变体中两种磷脂的缺失对呼吸作用没有实质性影响。在无细胞制备中，发现突变体中磷脂酰丝氨酸合成系统对丝氨酸的亲和力几乎比野生型低两个数量级。磷脂酰丝氨酸合成受损是突变细胞生长需要和磷脂组成异常的原因。
A single-gene nuclear choline-requiring mutant of Saccharomyces cerevisiae was studied. Choline as a growth supplement to synthetic media could be substituted by low concentrations of dimethylethanolamine, monomethylethanolamine or ethanolamine. DL-Serine also supported growth, but only at high concentrations: on a molar basis it was approximately one hundred times less effective than choline. When cultured in unsupplemented medium the mutant cells soon ceased to grow. The growth-arrested cells contained less than one fifth of the phosphatidylethanolamine present in wild-type cells and only traces of phosphatidylserine. The relative content of the two phospholipid species was raised by growing the mutant cells in the presence of choline of the other supplements but still remained lower than in wild-type cells. The mutant cells depleted of phosphatidylethanolamine and phosphatidylserine had greatly diminished ability to fuse with other cells in mating and their protoplasts showed increased resistance to hypotonic lysis. Respiration was not substantially affected by the deficit of the two phospholipid species in the mutant. In cell-free preparations, the affinity of the phosphatidylserine synthesizing system for serine was found to be almost two orders of magnitude lower in the mutant than in the wild-type. The impairment of phosphatidylserine synthesis accounts for growth requirement and the abnormal phospholipid composition of the mutant cells.