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Fig. 5 | Cell & Bioscience

Fig. 5

From: ISL1 controls pancreatic alpha cell fate and beta cell maturation

Fig. 5

Attenuated expression of insulin and a loss of glucagon producing cells during the secondary transition of pancreas development in Isl1CKO. a Quantitative RT-PCR analyses show reduced mRNA levels of endocrine hormones and increased expression of the transcription factor Fev in the E14.5 pancreas of Isl1CKO compared to controls. Data are presented as mean ± SEM (n = 8 pancreases per control, n = 7 pancreases per Isl1CKO), Unpaired t-test (****P < 0.0001, ***P < 0.001, **P < 0.01). b-g Representative sections from the control and Isl1CKO pancreas immunostained for glucagon (GCG), insulin (INS), PDX1 (differentiation marker of β cells), or alpha amylase (marker for exocrine cells) demonstrate loss of endocrine α cells (glucagon, GCG) in Isl1CKO. h, i Representative sections immunostained for proliferating cell nuclear antigen Ki67 in endocrine α (GCG) and β cells (INS). j Relative quantification of GCG+ and INS+ cells per α-amylase+ area (marker of exocrine tissue; n = 5 pancreases per genotype), and k the percentage of INS+ cells expressing Ki67 (n = 5 pancreases per genotype) and phosphorylated histone H3 (pHH3; n = 3 pancreases per genotype) per total number of INS+ cells is decreased in the Isl1CKO pancreas compared to littermate controls at E17.5. See also Additional file 1: Fig. S3. Data are presented as mean ± SD. Unpaired t-test (**P < 0.01, *P < 0.05, ns = not significant). Scale bars: 50 μm

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