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. 2010 Nov 15;286(3):2194–2204. doi: 10.1074/jbc.M110.186924

FIGURE 5.

FIGURE 5.

Lack of the C-terminal domain or the addition of a V232D mutation within the LRR fold decreases Tmod1 pointed end localization. The graph shows the percentage of myocytes demonstrating consistent, inconsistent, or diffuse filament pointed end localization (mean ± S.D.); categories are as described under “Experimental Procedures.” a, C-terminal domain truncation. Like WT GFP-Tmod1 (90.2 ± 2.0%), the majority of cells expressing GFP-Tmod1(1–344) (77.1 ± 0.6%) and (1–349) (97.2 ± 3.1%) demonstrated consistent pointed end localization, whereas Tmod1(1–320), which lacks the 6th C-terminal α-helix but contains the entire LRR fold, remarkably perturbed its localization at the pointed ends (14.0 ± 11.5%). Loss of the entire C-terminal domain (GFP-Tmod1(1–159)) resulted in no detectable localization at the pointed ends. b, C-terminal LRR point mutation. Cells expressing GFP-Tmod1(F263D) and GFP-Tmod1(L313D) demonstrated consistent localization at the pointed ends (71.3 ± 3.1% and 68.7 ± 2.3%, respectively). The percentage was lower in the cells expressing GFP-Tmod1(V232D) (52.0 ± 5.3%). Triple and double GFP-Tmod1 mutants (V232D/F263D/L313D, V232D/F263D, and V232D/L313D) further perturbed Tmod1 pointed end localization (0%, 13.3 ± 7.6%, and 10.7 ± 7.0%, respectively).