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Figure 4 | BMC Biology

Figure 4

From: Antagonistic roles in fetal development and adult physiology for the oppositely imprinted Grb10 and Dlk1genes

Figure 4

Whole body and relative organ weight analysis of neonates. A) Dlk1 +/p mice were significantly growth retarded whereas Grb10 m/+ and Grb10 m/+/Dlk1 +/p animals demonstrated whole body overgrowth when compared to wild type and Dlk1 +/p mice. Note, this graph is the same as that shown in Additional file 3: Figure S3A, reproduced here for convenience. B) Cranial sparing was observed, such that when brain weights were expressed as a percentage of total body weight Dlk1 +/p mice had proportionately enlarged brains in comparison to mice of all other genotypes. Conversely, the brains of Grb10 m/+ and Grb10 m/+/Dlk1 +/p animals were proportionately reduced in size compared to wild type and Dlk1 +/p mice (though note, not significantly so in the case of Grb10 m/+/Dlk1 +/p versus wild type animals). C) Grb10 m/+ and Grb10 m/+/Dlk1 +/p mice had disproportionally overgrown livers when compared to wild type and Dlk1 +/p animals. D) Kidney sparing was seen in both Grb10 m/+ and Grb10 m/+/Dlk1 +/p animals compared to wild type and Dlk1 +/p mice. Conversely, kidney weight was proportionately increased in Dlk1 +/p animals compared with mice of all other genotypes (though note, not significantly so in the case of Dlk1 +/p versus wild type animals). E) Overgrowth of lungs was noted in Dlk1 +/p mice compared to wild type mice. F) Proportionate growth of hearts was seen in all the analysed genotypes. G) Table summarising results of statistical analysis. All values represent means ± SEM, analysed using one way ANOVA with Tukey’s post-hoc analysis. WT n = 19, Dlk1 +/p n = 36, Grb10 m/+ n = 23, Grb10 m/+/Dlk1 +/p n = 22; * P <0.05; ** P <0.01; *** P <0.001. ANOVA, analysis of variance; SEM, standard error of the mean; WT, wild type.

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