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

Figure 4.

Figure 4

Loss of Tfb2m in β-cells leads to altered mitochondrial ultrastructure and impaired mitophagy. (A) Graph showing percentage of mitochondria with vesicular and swollen morphology in β-cells from control and β-Tfb2m−/− islets isolated from mice at 18 days of age. Representative electron micrograph showing normally shaped mitochondria in a control β-cell and vesicular and swollen mitochondria in β-Tfb2m−/− β-cell; control, n=34 images (4 mice), β-Tfb2m−/−, n = 40 images (3 mice). White arrows point to mitochondria. Scale bars: 0.5 μm. (B) Left – Representative fluorescence microscopy image of cells expressing LC3-GFP (green) from dispersed control and β-Tfb2m−/− islets after treatment with Mitotracker (red). Nucleus stained with DAPI (blue). Scale bars, 10 μm. Right – Quantification of LC3+ area co-localized with Mitotracker in control and β-Tfb2m−/− islets; control and β-Tfb2m−/−, 200 cells per condition was counted, n = 4 mice each at 18 days of age. (C) qRT-PCR analysis of Pdx1, Ins1, Ins2, and Slc2a2 mRNA in islets from control and β-Tfb2m−/− mice, n = 3 mice. Data are mean ± s.e.m. Statistical differences were examined by unpaired Student's t-test. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 versus the corresponding value for control mice.