The Smad-dependent TGFb and BMP signaling pathways have been well established for decades. TGFb or BMP ligands bind to (+)-JQ1 specific type II receptors to recruit the corresponding type I receptor to initiate a cascade of events leading to phosphorylation of their specific receptor-Smads. Generally, TGFb signaling depends on Smad2 and Smad3, while BMP signaling depends on Smad1, 5 and 8. The phosphorylated R-Smad forms a heterocomplex with the Smad4, the common partner Smad. The R-Smad/Co-Smad complex then translocates into the nucleus. Besides, TGFb/BMP signaling can also be mediated by noncanonical MAPK pathways, such as P38, JNK and Erk1/2 signaling pathways, during chondrogenesis. BMPs play an important role in the earliest stages of chondrogenesis, i.e. mesenchyme condensation and cell fate determination. In vitro BMPs can promote mesenchymal cells to differentiate into chondrocytes in high-density cultures in part by inducing Sox9 gene expression. Not surprisingly, BMP signaling components are highly expressed in growth plates with specific temporal-spatial patterns that correlate with functions during growth plate development and homeostasis.. For example, BMPs play an important role in regulating the proliferation of chondrocytes. Loss of Noggin, a potent BMP antagonist, leads to overgrowth of skeletal elements in mice. On the other hand, misexpression of Noggin in chick limbs causes reduction in of skeletal elements. Moreover, BMPs promote the differentiation of proliferating chondrocytes to hypertrophic chondrocytes, the chondrocyte specific expression of constitutively active Bmpr-1a in transgenic mice accelerated the maturation and hypertrophy of proliferating chondrocytes. Recently, Retting et al. showed that the complete loss of Smad1 and Smad5 in chondrocytes leads to a severe chondrodysplasia and that both mediators have overlapping functions in the developing growth plate. To further understand the role of BMP and TGFb signaling in the postnatal growth plate and to elucidate potential crosstalk between both signaling pathways we generated and compared two mouse models with partial deficiency of either BMP or TGFb signaling in the growth plate. Our findings showed that while reduced BMP signaling in proliferating chondrocytes leads to a shortening of the growth plate in part due to decreased cell proliferation, reduced TGFb signaling results in an increased proliferation rate and an elongated growth plate. We also identify an interesting interaction between these two signaling pathways in a cell model of chondrogenesis. The focus of this work has been compare the effects of BMP and TGFb signaling and interactions in chondrocytes and in postnatal cartilage. The essential requirements for these respective pathways have been successfully generated by strong loss of function phenotypes. However, because of early lethality of complete loss of signaling models, it was difficult to assess their requirements postnatally during homeostasis.