Fig. 3

Validation and phenotyping of Mvp-deficient mice. A Schematic representation of Mvp knockout model construction. The knockout mutants were obtained by a promoter gene trap design, resulting in the insertion of a β-galactosidase/neomycin phosphotransferase (β-GEO) cassette within the first intron of the Mvp gene. The polyA-tail (pA) serves to end the transcription and thus discard the transcription of Mvp gene. B Validation of Mvp knockout at the protein level using Western blot (WB) from liver extracts of Mvp^+/+ (n = 2), Mvp^+/− (n = 2), and Mvp^−/− (n = 3) mice. Actin was used as a loading control for normalization. For quantification, see Additional file 1: Fig. S6D. C Viability screen of Mvp knockout mice. Left: schematic representation of heterozygous-by-heterozygous breeding scheme, with expected Mendelian ratio of segregation of the offspring. Right: graph represents the ratio of each genotype of successfully genotyped mice obtained from heterozygous-by-heterozygous breeding (n = 617). D, E Graph showing the total brain area (1_TBA) measured at four time points, embryonic age 18.5 (E18.5), postnatal day 10 (P10), P45, and P120, in male (D) and female (E) Mvp^−/− mice (n = 5–7 in each group). F Half images of the coronal brain sections stained with Nissl-luxol at the four time points from male Mvp^+/+ and Mvp^−/− mice. Plots are shown as mean ± SEM. Two-tailed Student t test equal variance (D, E). *p < 0.05, **p < 0.01