Mitogen-activated Protein Kinase Kinase 1-dependent Golgi Unlinking Occurs in G2Phase and Promotes the G2/M Cell Cycle Transition

Brefeldin A
DOI: 10.1091/mbc.e06-06-0530 Publication Date: 2006-12-21T01:48:23Z
ABSTRACT
Two controversies have emerged regarding the signaling pathways that regulate Golgi disassembly at G(2)/M cell cycle transition. The first controversy concerns role of mitogen-activated protein kinase activator (MEK)1, and second participation structure in a novel "checkpoint." A potential simultaneous resolution is suggested by hypothesis MEK1 triggers unlinking late G(2) to control kinetics. Here, we show inhibition RNA interference or using MEK1/2-specific inhibitor U0126 delayed passage synchronized HeLa cells into M phase. requirement for normal mitotic entry was abrogated if proteins were dispersed before phase treatment with brefeldin GRASP65, which links stacks ribbon network, depleted. Imaging revealed apparatus begins phase, independent cyclin-dependent 1 activation, requires MEK signaling. Furthermore, expression GRASP family member GRASP55 after alanine substitution its MEK1-dependent phosphorylation sites inhibited both Thus, plays an vivo reorganization, regulates progression.
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