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. 2019 Jun 20;4(12):e127896. doi: 10.1172/jci.insight.127896

Figure 6. Upregulation of Kv2.1 restores the spatial organization of fusion sites in T2D β cells.

Figure 6

(A) In ND β cells, compared with the full-length channel (Kv2.1-WT), a clustering-deficient mutant (Kv2.1-ΔC318) reduced the uniformity of fusion events monitored by TIRF imaging of granule-targeted NPY-EGFP (n = 22, 26, and 24 cells from 3 donors). Cells expressing the channel constructs were identified by channel-tagged mCherry and compared to cells expressing mCherry alone. (B) In a subset of cells with equivalent rates of exocytosis (dashed box), (C) expression of Kv2.1-WT had little effect on the proportion of events within hotspots and (D) slightly increased their density, while Kv2.1-ΔC318 reduced the overall contribution of hotspots to exocytosis. (E–H) Same as A–D, but in T2D β cells (n = 12, 16, and 10 cells from 3 donors). Here, Kv2.1-WT rescued the compartmentalization of fusion events. (F) In a subset of cells with similar fusion frequency (dashed box), (G) the overall proportion of events occurring in these spatially restricted regions and (H) the density of these sites are unchanged by WT-Kv2.1. Significance was determined by Kruskal-Wallis 1-way ANOVA followed by (A and H) Mann-Whitney posttest or by (C–E and G) ANOVA and Bonferroni’s posttest. *P < 0.05; **P < 0.01; ***P < 0.001.