Extended Data Fig. 3: Validation of the notch-responsive cells as the source of the newly formed β-cells in juvenile fish.
From: MNK2 deficiency potentiates β-cell regeneration via translational regulation
a-e, CID661578.6 promotes β-cell neogenesis in juvenile fish. Single-plane confocal images of Tg(ins:GFP);Tg(tp1:H2BmCherry);Tg(ins:flag-NTR) pancreata from 1-month-old zebrafish treated with DMSO (a) or CID661578.6 (b). Briefly, 1-month-old zebrafish were incubated with MTZ (1 mM) for 24 hours to ablate β-cells followed by chemical treatment for 2 days. Pancreata are outlined with white dashed lines. Quantification of β-cells in the secondary islets in the tail of the pancreas (c) shows an increase in β-cell regeneration, and quantification of the overlap between the notch-responsive cell tracer and β-cell marker demonstrated an increase in the number of β-cells derived from notch-responsive cells (d). CID661578.6 treatment also doubled the ins+ area normalized to the body length of the fish (μm2/mm) (e). Scale bar, 50 µm. (c and d), n = 11 (Control) and n = 13 (CID661578.6); (e), n = 10 (Control) and n = 13 (CID661578.6). Unpaired two-tailed Student’s t test was used to assess significance for (c) *P = 0.0229; two-tailed Mann-Whitney test was used for (d) ****P < 0.0001; two-tailed Mann-Whitney test was used for (e) **P = 0.0099. Data are presented as mean values ±SEM.
