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MBC in Press, published online ahead of print April 23, 2008
Mol. Biol. Cell 10.1091/mbc.E07-11-1200

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Submitted on December 1, 2007
Revised on April 2, 2008
Accepted on April 14, 2008

GRASP55 Regulates Golgi Ribbon Formation

Timothy N. Feinstein and Adam D. Linstedt

Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213

Monitoring Editor: Benjamin Glick

Recent work indicates that MEK1 signaling at the G2/M cell cycle transition unlinks the contiguous mammalian Golgi apparatus and that this regulates cell cycle progression. Here we sought to determine the role in this pathway of GRASP55, a Golgi-localized target of MEK/ERK phosphorylation at mitosis. In support of the hypothesis that GRASP55 is inhibited in late G2 phase causing unlinking of the Golgi ribbon, we found that HeLa cells depleted of GRASP55 show a fragmented Golgi similar to control cells arrested in G2 phase. In the absence of GRASP55 Golgi stack length is shortened but Golgi stacking, compartmentalization, and transport appear normal. Absence of GRASP55 was also sufficient to suppress the requirement for MEK1 in the G2/M transition, a requirement which we previously found depends on an intact Golgi ribbon. Further, mimicking mitotic phosphorylation of GRASP55 using aspartic acid substitutions is sufficient to unlink the Golgi apparatus in a gene replacement assay. Our results implicate MEK1/ERK regulation of GRASP55-mediated Golgi linking as a control point in cell cycle progression.

Address correspondence to: Adam D. Linstedt (linstedt{at}andrew.cmu.edu)






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