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. Author manuscript; available in PMC: 2013 Apr 2.
Published in final edited form as: Cell. 2012 Jun 8;149(6):1339–1352. doi: 10.1016/j.cell.2012.04.028

Figure 7. STRIPAK Signaling Complexes Bridge the Nuclear Envelope, Centrosomes and Golgi.

Figure 7

(A,B) Flow cytometry analysis showing DNA content histograms of HeLa cells treated with control siRNA targeting Luciferase (black) or siRNAs to deplete SLMAP (Far10) or MOBKL3 (Mob1). HeLa cells depleted of the designated proteins and labled for immuno-fluorescence. See Fig S6 for additional images of siMOBKL3 phenotypes. (C) Fraction of interphase cells with abnormal numbers of pericentrin foci following siRNA treatment. Errors Bars = S.E.M. (D,E) HeLa cells transiently expressing mCherry-SLMAP and labeled for immuno-fluorescence. See Fig S7 for the lack of co-localization between mCherry-SLMAP and the Golgi. (F) Domain architecture of the FAR/STRIPAK components. (G) STRIPAK Model: Striatin and STRIPs reside at the Golgi. Striatins serve as regulatory B”' subunits of a PP2A trimer. Striatin/STRIP recruit MOBKL3, which directs Ste20/Germinal Center kinases. STRIPs interact with SLMAP in the outer nuclear membrane, bridging the Golgi, the centrosome, and the nuclear envelope. These interactions are likely restricted to specific cell cycle phases and the interaction between SLMAP and centrosomes predominates during mitosis. Disruption of STRIPAK leads to diverse failures during mitosis: including centrosome duplication errors, spindle assembly errors and cytokinesis failure.