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. 2017 May 19;6(7):651–663. doi: 10.1016/j.molmet.2017.05.005

Figure 5.

Figure 5

Loss of Tfb2m in β-cells leads to altered insulin ultrastructure and impaired autophagy. (A) Left – Representative fluorescence microscopy image of β-cells (stained for insulin – red) from control and β-Tfb2m−/− islets expressing LC3-GFP (green). Nucleus stained with DAPI (blue). Scale bars, 10 μm. Right – Quantification of total LC3+ area in control and β-Tfb2m−/− islets; control and β-Tfb2m−/−, n = 4 mice each at 18 days of age. (B) qRT-PCR analysis of Lamp2 and Ctsb mRNA in islets from control and β-Tfb2m−/− mice, n = 3 mice. (C) Left – Representative fluorescence microscopy image of cells expressing LC3-GFP (green) from control and β-Tfb2m−/− islets after treatment with Lysotracker (red). Nucleus stained with DAPI (blue). Scale bars, 10 μm. Right – Quantification of LC3+ area co-localized with Lysotracker in control and β-Tfb2m−/− islets; control and β-Tfb2m−/−, n = 4 mice each at 18 days of age. (D) qRT-PCR analysis of Ddit3 and Cebpb mRNA in islets from control and β-Tfb2m−/− mice, n = 3 mice. All data are mean ± s.e.m. Statistical differences were examined by unpaired Student's t-test. *P < 0.05, ***P < 0.001 and ****P < 0.0001 versus the corresponding value for control mice.