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. Author manuscript; available in PMC: 2016 Jul 19.
Published in final edited form as: Dev Biol. 2015 Dec 3;409(2):354–369. doi: 10.1016/j.ydbio.2015.12.003

Fig. 2.

Fig. 2

Insulin signaling blockade increases embryonic β cell formation. (A) Schematic of a dominant negative IRS2 construct designed to block transmission of insulin signaling; C-terminal effector binding domains are replaced with GFP. (B,C) 5 hpf embryo injected with dnIRS2-GFP mRNA (B) Photomicrograph of epifluorescence shows ubiquitous distribution of GFP. (C) Confocal plane shows the localization of dnIRS2-GFP to the plasma membrane while co-injected H2B-RFP mRNA labels cell nuclei red. (D, E) Confocal projections of control (D) and dnIRS2-GFP mRNA-injected islets in 24 hpf Tg(ins:dsRed) embryos. (F) Quantification of insa:dsRed+ β cells in 24 hpf control (n = 12) and dnIRS2-GFPmRNA injected embryos (n = 10). (G,H) Confocal projections of DMSO-treated control (G) and 1 µM wortmannin-treated islets in 30 hpf Tg(ins:CFP-NTR) embryos. (I) Quantification of β cells in DMSO-treated control (n = 18) and 1 µM wortmannin-treated (n = 17) islets in 30 hpf embryos. Student t-test was used to determine significance in F and I.