Pfanner N, Orci L, Glick B S, Amherdt M, Arden S R, Malhotra V, Rothman J E
Department of Biology, Princeton University, New Jersey 08544-1014.
Cell. 1989 Oct 6;59(1):95-102. doi: 10.1016/0092-8674(89)90872-6.
We describe a new role for fatty acylation. Conditions were established under which vesicular transport from the cis to the medial Golgi compartment in vitro depends strongly upon the addition of a fatty acyl-coenzyme A, e.g., palmitoyl-CoA. Using an inhibitor of long-chain acyl-CoA synthetase, we demonstrate that the fatty acid has to be activated by CoA to stimulate transport. A nonhydrolyzable analog of palmitoyl-CoA competitively inhibits transport. Electron microscopy and biochemical studies show that fatty acyl-CoA is required for budding of (non-clathrin-) coated transport vesicles from Golgi cisternae and that budding is inhibited by the nonhydrolyzable analog.
我们描述了脂肪酰化的一种新作用。建立了体外从顺式高尔基体向中间高尔基体区室进行囊泡运输强烈依赖添加脂肪酰辅酶A（例如棕榈酰辅酶A）的条件。使用长链酰基辅酶A合成酶抑制剂，我们证明脂肪酸必须被辅酶A激活才能刺激运输。棕榈酰辅酶A的一种不可水解类似物竞争性抑制运输。电子显微镜和生化研究表明，脂肪酰辅酶A是高尔基体潴泡产生（非网格蛋白）包被运输囊泡所必需的，且这种产生受到不可水解类似物的抑制。
