Fig. 3

Activating enhancer binding protein 2, epsilon, expression in articular cartilage and analysis of the cartilage layer in wild-type and Tfap2e ^−/− mice. a Activating enhancer binding protein 2, epsilon (AP-2ε) mRNA expression was measured in mesenchymal limb bud cells (LB) of embryonic day 11.5 (E11.5) embryos and in articular chondrocytes (AC) from the knee joints of 10.5-week-old (10.5 w) mice via quantitative RT-PCR. In the wild-type (WT) samples, a strong induction in the expression rate of the transcription factor was observed. As expected, when we used genotype-specific primers, normal AP-2ε mRNA without the neomycin insert could not be detected in corresponding Tfap2e ^−/− samples, serving as a negative control. b Histological sections through the knee joints of 10.5-week-old WT and Tfap2e ^−/− mice after staining with Safranin O/Fast Green (left). Morphologically, no obvious abnormalities between the two genotypes could be detected at this age. Furthermore, the thickness of the articular cartilage layer in the tibia and femur was similar in each genotype (right). c Exemplary pictures from the ultrastructural analysis of the articular cartilage layer in the knee joints of adult WT and Tfap2e ^−/− mice depicting chondrocytes (left) and the extracellular matrix (right). No obvious differences could be determined in a qualitative evaluation. The data are given as the means ± standard error of the mean. ns, Not significant; Tfap2e ^−/−, Deficient for activating enhancer binding protein 2, epsilon. ***P < 0.001. In (A), cells of four individual litters were used for LB and nine individual animals for AC. In (B), 14 WT and 15 Tfap2e ^−/− mice were compared. In (c), two mice were used for each genotype. Micrographs shown are derived from the middle and deep zones of the cartilage layer and were adjusted to equal magnification