BMPs bind tetrameric complexes of two type I and two type II transmembrane serine-threonine kinase receptors. Upon BMP binding, these complexes transduce a signal by phosphorylating members of the Smad family of transcription factors (Massague 1996). Recent experiments have implicated two different BMP type I receptors in skeletal patterning, BMPR1A and BMPR1B. Both receptors can bind BMP2, BMP4, and GDF5, although GDF5 shows higher affinity for BMPR1B (Koenig et al. 1994; ten Dijke et al. 1994; Yamaji et al. 1994; Nishitoh et al. 1996; Chalaux et al. 1998). Both receptors are also expressed in dynamic patterns during normal development. In limbs, Bmpr1a expression becomes restricted to joint interzones, perichondrium, periarticular cartilage, hypertrophic chondrocytes, and interdigital limb mesenchyme. In comparison, Bmpr1b expression is seen primarily in condensing precartilaginous mesenchymal cells, regions flanking joint interzones, perichondrium, and periarticular cartilage (Dewulf et al. 1995; Mishina et al. 1995; Zou et al. 1997; Baur et al. 2000). Null mutations in the Bmpr1b gene produce viable mice with defects in bone and joint formation that closely resemble those seen in mice missing Gdf5 (Storm and Kingsley 1996; Baur et al. 2000; Yi et al. 2000). Null mutations in Bmpr1a cause early embryonic lethality, with defects in gastrulation similar to those seen in mice with mutations in Bmp4 (Mishina et al. 1995; Winnier et al. 1995). Recent studies with floxed alleles suggest that Bmpr1a is also required for many later developmental events, but its roles in bone and joint formation have not yet been tested (Mishina 2003).