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. 2016 Jan 1;27(1):137–152. doi: 10.1091/mbc.E15-09-0650

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© 2016 Tang et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 2: — Mena regulates Golgi integrity through actin polymerization. (A) HeLa cells treated with indicated siRNA were stained for Mena and GRASP65. (B) Immunoblot of HeLa cells from A. (C) Quantification of A for the percentage of cells with fragmented Golgi. (D) Representative EM images of the cells described in A. Arrows, Golgi stacks. Bar, 500 nm. (E) Quantification of D for the average cisternal length of Golgi stacks. (F) Quantification of D for the average number of cisternae per Golgi stack. (G) Mena-depleted HeLa cells were transfected with a cDNA for GFP or GFP-tagged, RNAi-resistant Mena WT or mutants and stained for GRASP65. Bar, 20 μm (A, G). (H) Cells were transfected first with nonspecific (lane 1) or Mena-specific siRNA (lanes 2–5) and then with plasmid of GFP (lane 2), GFP-tagged, RNAi-resistant Mena WT (lane 3), ΔFAB (lane 4), and ΔGAB (lane 5) mutants and analyzed by Western blot. endo. Mena, endogenous Mena. (I) Quantification of the percentage of GFP-positive cells with fragmented Golgi in G. ***p < 0.001.