Leber R, Zinser E, Hrastnik C, Paltauf F, Daum G
Institut für Biochemie und Lebensmittelchemie, Technische Universität Graz, Austria.
Biochim Biophys Acta. 1995 Mar 8;1234(1):119-26. doi: 10.1016/0005-2736(94)00270-y.
Fatty acyl esters of the yeast specific sterol, ergosterol, are exclusively stored in lipid particles. Under conditions of sterol deficiency, e.g., in the presence of terbinafine, an inhibitor of fungal squalene epoxidase, steryl esters are hydrolyzed, and sterols are set free for membrane formation. Lipid particles do not contain steryl-ester hydrolase activity themselves; the highest specific activity of this enzyme is found in the plasma membrane. Therefore, steryl esters have to be exported from lipid particles to their site of hydrolytic cleavage. This process of translocation and metabolic conversion was studied in vivo. Addition of nocodazole to terbinafine-treated cells did not disturb the mobilization of steryl esters, indicating that this process is not mediated by microtubuli-dependent vesicle flux. Under the influence of inhibitors of cellular energy production (azide and fluoride) and protein biosynthesis (cycloheximide) mobilization of steryl esters came to an halt. These results support the view that ongoing membrane proliferation may be a driving force for the release of sterols from steryl esters of lipid particles.
酵母特异性甾醇麦角甾醇的脂肪酰酯专门存储在脂质颗粒中。在甾醇缺乏的条件下，例如在存在真菌角鲨烯环氧酶抑制剂特比萘芬的情况下，甾醇酯会被水解，甾醇被释放出来用于膜的形成。脂质颗粒本身不含有甾醇酯水解酶活性；该酶的最高比活性存在于质膜中。因此，甾醇酯必须从脂质颗粒转运到其水解切割位点。在体内研究了这种转运和代谢转化过程。向经特比萘芬处理的细胞中添加诺考达唑不会干扰甾醇酯的动员，这表明该过程不是由微管依赖性囊泡通量介导的。在细胞能量产生抑制剂（叠氮化物和氟化物）和蛋白质生物合成抑制剂（环己酰亚胺）的影响下，甾醇酯的动员停止。这些结果支持这样一种观点，即持续的膜增殖可能是脂质颗粒中甾醇从甾醇酯释放的驱动力。
