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. 2012 Mar 19;196(6):727–742. doi: 10.1083/jcb.201107096

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© 2012 Ryan et al.

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Figure 7. — Impaired MT acetylation results in Golgi fragmentation after loss of dystonin-a2. (A) Silencing of dystonin-a2 in 293T cells results in decreased MT acetylation coupled with reorganization of the Golgi complex. cis-Golgi (GM130) tightly associates with Ac–α-tubulin (arrows vs. arrowheads). (B) 3D rendering of P15 primary sensory neurons from WT and dt^27J mice. dt^27J sensory neurons show reduced Ac–α-tubulin coupled to a decrease GM130 antigenic labeling in the cell soma. (C and D) Maintenance of MT acetylation status with TSA prevents Golgi fragmentation after depletion of dystonin-a2 (ANOVA posthoc Tukey; *, P < 0.05; n = 6). Arrows depict compact Golgi, whereas arrowheads depict dispersed Golgi. (E) Nocodazole washout of 293T cells after dystonin-a2 depletion shows that MT nucleation from the centrosome is moderately delayed after dystonin-a2 depletion but not dystonin-a1 silencing. Arrows identify sites of MT polymerization. After dystonin-a2 silencing, centrosomal MT polymerization is impeded (arrowhead). Error bars show means ± SEM. Cont, control; Tub, tubulin. Bars, 10 µm.