An unsaturated fatty acid mutant of Chinese hamster V79

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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.