Figure 5.
Figure 5. DP–EB1 interactions are impaired by disease mutations in the DP N terminus. (A) PLA of EB1 with WT and mutated DPII-GFP constructs in SCC9 cells transfected with siRNA targeting the 3′ UTR of endogenous DP. Color panels show PLA dots overlaid with GFP expression. Boxed regions in color overlays are magnified in the panels on the right. PLA values are quantified in the graph (A′; n = 12 image fields from three independent experiments). Bars: (main images) 10 µm; (insets) 5 µm. Error bars indicate SEM. (B) Radar plots: EB1 comet angles categorized for frequencies between 0 and 90° relative to cell–cell contacts in cells expressing WT and mutated DPII-GFP in the background of endogenous DP (n > 250 comets per condition from three independent experiments). Results are compiled in a cumulative frequency plot below the individual graphs, with the x axis representing frequency bins for EB1 angles. All data are from SCC9s.

DP–EB1 interactions are impaired by disease mutations in the DP N terminus. (A) PLA of EB1 with WT and mutated DPII-GFP constructs in SCC9 cells transfected with siRNA targeting the 3′ UTR of endogenous DP. Color panels show PLA dots overlaid with GFP expression. Boxed regions in color overlays are magnified in the panels on the right. PLA values are quantified in the graph (A′; n = 12 image fields from three independent experiments). Bars: (main images) 10 µm; (insets) 5 µm. Error bars indicate SEM. (B) Radar plots: EB1 comet angles categorized for frequencies between 0 and 90° relative to cell–cell contacts in cells expressing WT and mutated DPII-GFP in the background of endogenous DP (n > 250 comets per condition from three independent experiments). Results are compiled in a cumulative frequency plot below the individual graphs, with the x axis representing frequency bins for EB1 angles. All data are from SCC9s.

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