Signaling via mitogen-activated protein kinase kinase (MEK1) is required for Golgi fragmentation during mitosis
Signaling via mitogen-activated protein kinase kinase (MEK1) is required for Golgi fragmentation during mitosis
复制标题
DOI：
10.1016/s0092-8674(00)80913-7
复制
发表时间：
1998-01-23
期刊：
影响因子：
64.5
通讯作者：
Malhotra, V
中科院分区：
文献类型：
--
作者：
Acharya, U;Mallabiabarrena, A;Malhotra, V
我们已经开发了一种检测方法，使用透化细胞监测分裂过程中发生的高尔基复合体的碎片。高尔基堆叠，在透化间期正常大鼠肾（NRK）细胞，孵育后，有丝分裂提取物进行广泛的碎片化，和破碎的高尔基膜分散在整个细胞质。我们发现，继续存在的p34（cdc2），有丝分裂起始激酶，是没有必要的高尔基体片段。相反，片段化依赖于胞质有丝分裂原活化蛋白激酶激酶1（MEK1或MAPKK1）。然而，MEK1、ERK 1和ERK 2的已知细胞质底物对于该过程不是必需的。有趣的是，我们发现了一个高尔基体相关的ERK，我们建议在高尔基体碎片的MEK 1的可能目标。
We have developed an assay using permeabilized cells to monitor fragmentation of the Golgi complex that occurs during mitosis. Golgi stacks, in permeabilized interphase normal rat kidney (NRK) cells, upon incubation with mitotic extracts undergo extensive fragmentation, and the fragmented Golgi membranes are dispersed throughout the cytoplasm. We find that the continued presence of p34(cdc2), the mitosis initiation kinase, is not necessary for Golgi fragmentation. Instead, fragmentation depends on cytosolic mitogen-activated protein kinase kinase 1 (MEK1 or MAPKK1). However, the known cytoplasmic substrates for MEK1, ERK1, and ERK2 are not required for this process. Interestingly, we find a Golgi-associated ERK, which we propose as the likely target for MEK1 in Golgi fragmentation.