Fig. 3 | Nature Communications

Fig. 3

From: Signal peptide represses GluK1 surface and synaptic trafficking through binding to amino-terminal domain

Fig. 3

GluK1 ATD is required to restrain its synaptic targeting. a–d The eEPSCs measured at −70 mV for chimera receptors biolistically expressed in CA1 neurons vs. neighboring control neurons. The scale bars for representative eEPSC traces were 200 pA/25 ms for a, b and 100 pA/25 ms for c, d. Bar graphs show normalized eEPSC amplitudes (mean ± SEM) presented in scatter plots (a GluK2(SPGluK1), n = 13, 1270.14 ± 222.55% control, ***p < 0.0005; b GluK2(N71GluK1), n = 14, 939.65 ± 204.54% control, ***p < 0.0001; c GluK2(N137GluK1), n = 20, 1270.14 ± 296.59% control, **p < 0.005; d GluK1(N71-136GluK2), n = 17, 305.77 ± 29.94% control, ***p < 0.0005.) Statistical analyses are comparisons between transfected neurons and respective control neurons using two-tailed Wilcoxon signed-rank sum test. e Bar graph shows logarithm summary of the eEPSC amplitude ratios (mean ± SEM) between the experimental and respective control neurons for the indicated transfections (GluK2: 1.25 ± 0.07; GluK2(SPGluK1): 1.14 ± 0.10; GluK2(N71GluK1): 1.03 ± 0.12; GluK2(N137GluK1): 0.38 ± 0.11; GluK2(ATRGluK1): ***p < 0.0001 compared to wild-type GluK2. GluK1: 0.03 ± 0.10; GluK1(N71-136GluK2): 0.57 ± 0.07; ###p < 0.0005). It should be noted that the raw data of GluK1, GluK2 and GluK2(ATRGluK1) are re-used from our previous study15. The schematic cartoons for the swapped domains between GluK1 (blue) and GluK2 (red) proteins are shown below the graph. Data in e are analyzed using Mann–Whitney U-test

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