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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Semin Cell Dev Biol. 2009 Sep;20(7):793–800. doi: 10.1016/j.semcdb.2009.03.016

Fig. 2. Control of Golgi PI(4)P during cell growth.

Fig. 2

(A): Metabolic control of Golgi PI(4)P in yeast. In the presence of sufficient glucose, exponentially growing yeast exhibit high Golgi PI(4)P levels generated by Pik1p/Frq1p. Under these conditions, the lipid phosphatase Sac1p localizes to the ER in a complex with Dpm1p. Glucose starvation triggers translocation of Sac1p to the Golgi and release of Pik1p/Frq1p from Golgi membranes. The cytosolic Pik1p/Frq1p complex binds to 14-3-3 proteins encoded by BMH1 and BMH2. (B): Mitogen-dependent control of PI(4)P in mammalian cells. In mitogen stimulated cells, SAC1 lipid phosphatase remains largely localized at the ER, which allows for increased levels of PI(4)P at the Golgi synthesized by PI4KIIα and PI4KIIIβ. During serum starvation and in quiescent cells, SAC1 oligomerizes and accumulates in the Golgi, which in turn down-regulates Golgi PI(4)P and slows constitutive secretion. Whether PI4KIIα and PI4KIIIβ remain associated with the Golgi under these conditions is unknown.