Fig. 1. Targeted disruption of the Pten gene in mouse chondrocytes results in skeleton overgrowth. (A) Phenotype of Pten^+/+;Col2a1-Cre (left), Pten^Co/+;Col2a1-Cre (middle) and Pten^Co/Co;Col2a1-Cre (right) littermates at P40. (B) Tail length measurements of female (left) and male (right) mice at various time points. Each point represents the mean ±s.d. from six mice. (C) Soft X-ray images of femur and tibia from P50 mice showing increased width (red arrowheads) and bone density (white arrowheads) of long bones in mutant mice. (D) Tibia and femur length were not significantly changed in mutant mice. Mean ±s.d. of eight samples from four mice of each genotype. P>0.05. (E-G) Efficient deletion of Pten in mutant cartilage as revealed by immunohistochemistry (E), Southern blot (F) and western blot (G). Loss of Pten also caused phosphorylation of AKT (p-AKT) within chondrocytes (E,G). Scale bar: 50 µm.