Extended Data Fig. 4: Newly-derived β-cells express mnx1, another marker for β-cell identity/maturation, and are devoid of glucagon expression.
From: MNK2 deficiency potentiates β-cell regeneration via translational regulation
a-d, Single-plane confocal images of 6 dpf Tg(mnx1:GFP);Tg(ins:flag-NTR) larvae treated with DMSO (a) or CID661578 (b) (4-6 dpf) after β-cell ablation (3-4 dpf) and staining for insulin. Quantification results showed that CID661578 treatment increased the number of β-cells (c), but there was no difference in the percentage of mnx1:GFP+, insulin+ β-cells (d). Scale bar, 10 µm. For (c and d) n = 10 (Control) and n = 12 (CID661578). Unpaired two-tailed Student’s t test was used to assess significance for (c) *P = 0.0497. Data are presented as mean values ±SEM. e-g, Representative confocal images of 6 dpf Tg(ins:H2BGFP);Tg(tp1:H2BmCherry);Tg(ins:flag-NTR) larvae treated with DMSO (e) or CID661578.6 (f) (4-6 dpf) after β-cell ablation (3-4 dpf) and stained for glucagon. White arrowheads point to bihormonal cells (glucagon+, ins:H2BGFP+) derived from notch-responsive cells. Quantification of bihormonal cells derived from notch-responsive cells (g) showed no difference between treatments. Scale bar, 10 µm. n = 9 (Control) and n = 7 (CID661578.6). Data are presented as mean values ±SEM.
