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A more recent version of this article appeared on February 1, 2007
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Submitted on June 19, 2006
Revised on November 22, 2006
Accepted on November 30, 2006
Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213
Monitoring Editor: Benjamin Glick
Two controversies have emerged regarding the signaling pathways that regulate Golgi disassembly at the G2/M cell cycle transition. The first concerns the role of MAP kinase activator MEK1 and the second concerns the participation of Golgi structure in a novel cell cycle "checkpoint." A potential simultaneous resolution is suggested by the hypothesis that MEK1 triggers Golgi unlinking in late G2 to control G2/M kinetics. Here we show that inhibition of MEK1 by RNA interference or by using the MEK1/2-specific inhibitor U0126 delayed the passage of synchronized HeLa cells into M-phase. The MEK1 requirement for normal mitotic entry was abrogated if Golgi proteins were dispersed before M-phase by treatment of cells with brefeldin A or if GRASP65, which links Golgi stacks into a ribbon network, was depleted. Imaging revealed that unlinking of the Golgi apparatus begins before M-phase, is independent of CDK1 activation and requires MEK signaling. Further, expression of the GRASP family member GRASP55 after alanine substitution of its MEK1-dependent mitotic phosphorylation sites inhibited both late-G2 Golgi unlinking and the G2/M transition. Thus, MEK1 plays an in vivo role in Golgi reorganization which regulates cell cycle progression.
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