An unsaturated fatty acid mutant of Chinese hamster V79

从中国仓鼠V79细胞中分离V79-UF细胞，作为需要外源不饱和脂肪酸生长的细胞系。V79-UF中单烯脂肪酸形成的减少是由于缺乏硬脂酰-CoA去饱和酶的刺激，该酶是将饱和脂肪酸转化为单烯脂肪酸的关键酶。V79-UF细胞将花生四烯酸掺入磷脂中。由此形成的多不饱和磷脂分子种类以比质膜更高的量分布在细胞内膜中。质膜流动性不受磷脂酰胆碱/磷脂酰乙醇胺比例的控制，但胆固醇的积累。因此，据推测，胆固醇从内质网向质膜的单向运输导致内质网中胆固醇的损失，使得内质网的流动性异常。这种变化可能导致细胞致命。

V79-UF cells were isolated from Chinese hamster V79 cells as a cell line that requires exogenous unsaturated fatty acid for growth. The reduced formation of monoenoic fatty acids in V79-UF was due to deficiency in the stimulation of stearoyl-CoA desaturase which is a key enzyme to convert saturated fatty acids to monoenoic fatty acids. V79-UF cells incorporated arachidonic into phospholipids. Polyunsaturated phospholipid molecular species thus formed were distributed in a higher amount in the intracellular membrane than in plasma membrane. Plasma membrane fluidity was not controlled by the phosphatidylcholine/phosphatidylethanolamine ratio, but by accumulation of cholesterol. Hence, it is postulated that the loss of cholesterol in the endoplasmic reticulum by the one-way direction of cholesterol transport from the endoplasmic reticulum to plasma membrane makes fluidity of the endoplasmic reticulum abnormal. Such change may cause the cells lethal.