By 1 wk after birth, obvious differences began to be detected in the articular regions of mutant animals. The expression of Col2a1 was reduced throughout the articular surfaces of the carpals, metacarpals, and phalanges of the forefeet (unpublished data). Less severe reductions were also seen in articular cells of tarsals and metatarsals in the hindfeet (unpublished data). By 2 wk of age, Col2a1 expression was reduced in most cells of the articular region (Figure 5L and 5Q), accompanied by markedly reduced Safranin O staining (Figure 5K and 5P), and decreased expression of Agg and two genes normally expressed in more mature articular cartilage cells, Collagen 3 (Col3a1) and Collagen 10 (Col10a1) (Figure 5M and 5R) (unpublished data) (Eyre 2002). Inhibition of BMP signaling in cultured chondrocytes has previously been reported to induce Collagen 1 (Col1a1) expression, increase proliferation, and result in cells with flattened, fibroblast-like morphology (Enomoto-Iwamoto et al. 1998). However, we saw no increase in the expression of Col1a1 in mutant articular cartilage, and no proliferation was detected in articular cells of either mutant or control animals (unpublished data). While recombined LACZ marker expression was detected in most articular cartilage cells, it was also observed in scattered subarticular chondrocytes, growth plate chondrocytes, and osteoblasts (Figure 5O and 5T) (unpublished data). Although this implies that BMP signaling was defective in multiple cell types, the observed defects were confined to the articular cartilage. For example, Osteocalcin and Col1a1 expression appeared normal in osteoblasts (unpublished data). Together, these data suggest that BMPR1A activity is required in postnatal joint articular cartilage to maintain expression of many genes encoding structural components of cartilage matrix.