Kasai R, Kitajima Y, Martin C E, Nozawa Y, Skriver L, Thompson G A
Biochemistry. 1976 Nov 30;15(24):5228-33. doi: 10.1021/bi00669a005.
Further studies on the molecular mechanisms of temperature acclimation have been carried out using the ciliate Tetrahymena pyriformis. The most prominent change in lipid metabolism during acclimation to high temperature--depression of fatty acid desaturase activity--could be simulated by supplementing the growth medium of isothermally-grown cells with polyunsaturated fatty acids. Such cells resisted the membrane-fluidizing effect of the incorporated exogenous acids by increased use of de novo synthesized saturated acids in their phospholipids. The data support the conclusions arising from earlier experiments with temperature-shifted cells (Martin, C.E., Hiramitsu, K., Kitajima, Y., Nozawa, Y., Skriver, L., and Thompson, G.A., Jr. (1976), Biochemistry 15), showing that, when membrane fluidity increased to a superoptimal level, the activity of membrane-associated fatty acid desaturases was decreased. Since the reaction is controlled by membrane fluidity, rather than temperature per se, we postulate that it is the general mechnaism employed by cells adjusting to any fluidity-modifying factor, such as cations, drugs, etc.
利用梨形四膜虫对温度适应的分子机制进行了进一步研究。在适应高温过程中脂质代谢最显著的变化——脂肪酸去饱和酶活性降低——可以通过向等温生长细胞的生长培养基中添加多不饱和脂肪酸来模拟。这类细胞通过在其磷脂中更多地使用新合成的饱和脂肪酸来抵抗掺入的外源酸的膜流化效应。这些数据支持了早期对温度转换细胞实验得出的结论（Martin, C.E., Hiramitsu, K., Kitajima, Y., Nozawa, Y., Skriver, L., and Thompson, G.A., Jr. (1976), Biochemistry 15），表明当膜流动性增加到超最佳水平时，膜相关脂肪酸去饱和酶的活性会降低。由于该反应是由膜流动性控制的，而不是温度本身，我们推测这是细胞适应任何改变流动性的因素（如阳离子、药物等）所采用的一般机制。
