Skip to main content
. 2011 Jan 15;138(2):359–370. doi: 10.1242/dev.052324

Fig. 5.

Fig. 5.

CamkII acts partly through β-catenin. (A-C) Sections of chick growth plate cartilage either uninfected (A) or infected with RCAS(A)-HA-daCamkII (B), RCAS(A)-Wnt5a or RCAS(A)-dnFzd7 (C) were analyzed by immunofluorescence for HA-daCamkII (B), pCamkII (C) and β-catenin (A-C). (A) β-catenin is readily detected in nuclei (arrows) of wild-type prehypertrophic and hypertrophic chondrocytes (n=3). Bracket indicates prehypertrophic zone (PHZ). PC, proliferative chondrocytes. (B) Many RCAS(A)-HA-daCamkII-infected proliferative chondrocytes (white arrows; n=8) show high levels of nuclear β-catenin (red). (C) Ectopic Wnt5a expression reduces both pCamkII (green) and nuclear β-catenin (green) signals (n=3), whereas ectopic expression of dnFzd7 promotes both pCamkII (green) and nuclear β-catenin (n=3), consistent with co-regulation of these proteins by Wnt signaling. Red signal is the actin cytoskeleton, which is reduced in hypertrophic chondrocytes. (D-F) The effect of loss of β-catenin function on pCamkII and chondrocyte maturation was examined in Ctnnb1 mutant embryos. Trichrome staining revealed similar organization of growth plate chondrocytes in wild-type and Ctnnb1 mutant samples, although a lower cell density is observed in mutants (data not shown). The size of the prehypertrophic zone (Ihh; red line) relative to the length of the growth plate is similar (P>0.05) in wild-type (0.17 ± 0.02 mm; n=10) and mutant (0.19 ± 0.009 mm; n=10) samples (E). No obvious differences (P>0.05) in nuclear enrichment of pCamkII were detected between wild-type (59 ± 11%; n=8) and mutant (56 ± 8.9%; n=3) growth plates (F). Error bars indicate s.d. Scale bars: 100 μm in A; 50 μm in B; 200 μm in C; 300 μm in D.