Figure 1.

Loss of KLF3 results in up-regulation of the human α-globin gene in a transgenic mouse model. Line3 mice, containing a GFP transgene under the control of the human α-globin proximal promoter and HS-40 enhancer [22], were crossed with Klf3+/− mice to generate Line3::Klf3+/+, Line3::Klf3+/− and Line3::Klf3−/− mice, all homozygous for the transgene. Erythroid GFP fluorescence was then measured by flow cytometry. Shown are representative fluorescence profiles of (A) peripheral blood from mice at 3 weeks of age and (B) TER119+ sorted erythrocytes from embryonic day E14.5 fetal liver. The populations were gated to identify cells expressing low, intermediate and high levels of GFP. Statistical analysis of these gated populations is shown for (C) erythrocytes from mice at 3 weeks of age and (D) TER119+ fetal liver cells. For erythrocytes analyzed at 3 weeks of age, n = 32 for Line3::Klf3+/+, n = 48 for Line3::Klf3+/− and n = 8 for Line3::Klf3−/−. For the analysis of fetal erythrocytes, n = 3 for Line3::Klf3+/+and n = 4 for Line3::Klf3−/−. Error bars represent standard deviation and * represents P < 0.05 (two tailed t-test).

Funnell et al. BMC Molecular Biology 2014 15:8   doi:10.1186/1471-2199-15-8
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