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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Dev Biol. 2015 Mar 20;402(1):81–97. doi: 10.1016/j.ydbio.2015.03.007

Fig. 6. IPD-derived secondary endocrine cells, formed in response to inhibition of Notch signaling, are sensitive to Neurod knockdown.

Fig. 6

Experimental schedule (top); Tg(neurod:EGFP) control and Neurod morphant larvae were treated with 3 μM RO4929097 (γ-secretase inhibitor) from 3 to 6 dpf. Confocal images (merged z-stacks) of representative 6 dpf Tg(neurod:EGFP) untreated specimen (A, E), γ-secretase inhibitor treated specimen (B, F), γ-secretase inhibitor treated Neurod ATG morphant [1 ng] (C, G) and γ-secretase inhibitor treated Neurod UTR morphant [2ng] (D, H). Whole mount immunolabeling for GFP (green) and glucagon (red) (A–D) or for GFP (green) and insulin (red) (E–H). Mean (± s.d.) number of cells expressing glucagon (I) or insulin (J) from 4 independent experiments and from a minimum of 40 and 25 larvae per group, respectively. *, P<0.0001; t-test, two-tailed distribution. Primary endocrine islet (arrow), IPD-derived endocrine cells (red line). Magnification is different in panel A than in B–H. Scale bar = 20 μm.