Lippincott-Schwartz J, Donaldson J G, Schweizer A, Berger E G, Hauri H P, Yuan L C, Klausner R D
National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.
Cell. 1990 Mar 9;60(5):821-36. doi: 10.1016/0092-8674(90)90096-w.
Characteristics of brefeldin A (BFA)-induced redistribution of Golgi proteins into the endoplasmic reticulum (ER) and its relationship to an ER retrieval pathway were investigated. Retrograde movement of Golgi proteins into the ER occurred via long, tubulovesicular processes extending out of the Golgi along microtubules. Microtubule-disrupting agents (i.e., nocodazole), energy poisons, and reduced temperatures inhibited this pathway. In BFA-treated cells Golgi proteins appeared to cycle between the ER and an intermediate compartment marked by a 53 kd protein. Addition of nocodazole disrupted this dynamic cycle by preferentially inhibiting retrograde movement, causing Golgi proteins to accumulate in the intermediate compartment. In the absence of BFA, such an ER cycling pathway appeared to be followed normally by the 53 kd protein but not by Golgi proteins, as revealed by temperature shift experiments. We propose that BFA induces the interaction of the Golgi with an intermediate "recycling" compartment that utilizes a microtubule-dependent pathway into the ER.
研究了布雷菲德菌素A（BFA）诱导的高尔基体蛋白重新分布到内质网（ER）中的特征及其与内质网回收途径的关系。高尔基体蛋白通过沿着微管从高尔基体延伸出的长管状小泡过程逆行进入内质网。破坏微管的药物（即诺考达唑）、能量毒物和降低温度会抑制该途径。在BFA处理的细胞中，高尔基体蛋白似乎在内质网和由一种53kd蛋白标记的中间区室之间循环。添加诺考达唑通过优先抑制逆行运动破坏了这种动态循环，导致高尔基体蛋白积聚在中间区室。温度转换实验表明，在没有BFA的情况下，这种内质网循环途径似乎通常由53kd蛋白遵循，而不是由高尔基体蛋白遵循。我们提出，BFA诱导高尔基体与一个中间“回收”区室相互作用，该中间区室利用依赖微管的途径进入内质网。
