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Figure 10


Fig. 10. Model illustrating the phenotypic consequences of Kif3a deficiency. In a wild-type (WT) synchondrosis growth plate, Ihh would produce a physiologically restricted gradient (red) from the pre-hypertrophic zone (phz) into the flanking perichondrium and the preceding proliferative zone (pz). The upper limit of this restricted field of action would be set by Patched 1 and syndecan 3 (and other heparan sulfate proteoglycans), and would allow the normal proliferation of chondrocytes and the normal formation of intramembranous bone. In Kif3a-deficient (Kif3a-/-) growth plates, however, the Ihh distribution gradient would be expanded because of the marked reduction of syndecan 3 and Patched 1 expression. As a consequence, the topography of hedgehog signaling and action would be altered as well. Within the growth plate, Ihh signaling would be feeble, causing abnormal behavior of chondrocytes. In perichondrial tissues, Ihh signaling would be abnormally high and widespread, triggering excessive intramembranous bone deposition and ectopic cartilage formation. phz, pre-hypertrophic zone; pz, proliferative zone; WT, wild type.





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